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Simple Summary: The development and use of migrastatic drugs could help improve the outcomes for patients with high-grade non-muscle-invasive bladder cancer and muscle-invasive bladder cancer by inhibiting bladder cancer cell invasion and thereby decreasing the likelihood of disease progression and metastasis. A key barrier to this is the lack of suitable models to assess bladder cancer cell invasiveness. Here, we describe a bladder cancer-on-a-chip model. We demonstrate that our model supports the retention of the bladder cancer cell phenotype and can be used to reproducibly assess and quantify the invasiveness of live bladder cancer cells. Treatment with ATN-161, a well-known migrastatic drug, caused a dose-dependent decrease in bladder cancer cell invasiveness thereby validating the ability of our model to test migrastatic drugs. To our knowledge, a bladder cancer-on-a-chip model that can specifically assess bladder cancer invasiveness has not previously been described. We have developed a bladder cancer-on-a-chip model which supports the 3D growth of cells and can be used to assess and quantify bladder cancer cell invasiveness in a physiologically appropriate environment. Three bladder cancer cell lines (T24, J82, and RT4) were resuspended in 50% Matrigel® and grown within a multi-channel organ-on-a-chip system. The ability of live cells to invade across into an adjacent 50% Matrigel®-only channel was assessed over a 2-day period. Cell lines isolated from patients with high-grade bladder cancer (T24 and J82) invaded across into the Matrigel®-only channel at a much higher frequency compared to cells isolated from a patient with low-grade cancer (RT4) (p < 0.001). The T24 and J82 cells also invaded further distances into the Matrigel®-only channel compared to the RT4 cells (p < 0.001). The cell phenotype within the model was maintained as assessed by cell morphology and immunohistochemical analysis of E-cadherin. Treatment with ATN-161, an α5β1 integrin inhibitor and well-known migrastatic drug, caused a dose-dependent decrease in the invasiveness of the J82 cells (p < 0.01). The combined data demonstrate that our bladder cancer-on-a-chip model supports the retention of the bladder cancer cell phenotype and can be used to reproducibly assess and quantify the invasiveness of live bladder cancer cells. [ABSTRACT FROM AUTHOR]

Objective Biochemical remission rates of endoscopic endonasal transsphenoidal surgery (EETS) and its associated predictive factors were evaluated in patients with somatotrophin pituitary adenomas. Methods The patients who underwent EETS in Jinling Hospital were identified between 2011 and 2020. The surgeons' experience, preoperative insulin-like growth factor 1 (IGF-1), basal growth hormone (GH) levels, nadir GH levels, and the tumor characteristics were analyzed for their relationships with endocrine outcomes. Total 98 patients were included for single factor analysis and regression analysis. They were divided into three groups according to the admission chronologic order. Results The overall remission rate of the patients was 57% (56/98) for all the patients over 10 years. In the single factor analysis, we found that the tumor size, cavernous invasion, and sellar invasion were valuable to predict the endocrine outcome after surgery. As for the suprasellar invasion, no significant difference was found between the noninvasive group and the invasive group. The preoperative IGF-1 level (p = 0.166), basal GH level (p = 0.001), and nadir GH level (p = 0.004) were also different between the remission group and the nonremission group in the single factor analysis. The logistic regression analysis indicated that the preoperative nadir GH (odds ratio = 0.930, 95% confidence interval = 0.891–0.972, p = 0.001) was a significant predictor for the endocrine outcomes after surgery. Conclusion The surgeons' experience is an important factor that can affect the patients' endocrine outcomes after surgery. The macroadenomas with lateral invasion are more difficult to cure. Patients with higher preoperative nadir GH levels are less likely to achieve remission. [ABSTRACT FROM AUTHOR]

Background and Objectives: Aged red blood cell (RBC) transfusions in lung cancer patients are often related to cancer recurrence and shorter lifespans. Extracellular vesicles (EVs) accumulated in stored RBC suspensions may be one of the important influential factors. This study aims to investigate how EVs derived from RBC suspensions affect the progress of lung cancer through the most enriched microRNAs (miRNAs) previously reported in our research. Study Design and Methods: EVs derived from stored RBC suspensions in Weeks 1, 3 and 5 were harvested via ultracentrifugation. Lung adenocarcinoma H1975 cells were co‐cultured with EVs and transfected with miR1246 and miR150‐3p mimics to evaluate alterations in their proliferation, invasion and migration abilities in vitro. Proteomics and bioinformatics were performed to predict the signalling pathway related to invasion and migration of H1975, which were verified by western blotting (WB) and flow cytometry. Results: EVs derived from stored RBC suspensions in Weeks 3 and 5 could significantly enhance the invasion and migration ability of H1975 cells and also increase the expression of miR1246 and miR150‐3p. After transfection with miR1246 and miR150‐3p mimics, invasion, migration and proliferation of H1975 cells were obviously enhanced. Proteomics analysis demonstrated that EVs co‐cultivation and miRNA transfection groups were both enriched in cell adhesion molecules. WB and cytometry indicated that integrin beta‐1 (ITGB1) and Rap1b were increased. Conclusions: EVs derived from stored RBC suspensions can enhance invasion and migration ability of lung cancer cells via the most accumulated miR1246 and miR150‐3p, which may increase the expression of ITGB1 through Rap1 signalling pathway. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is the most prevalent type of hematopoietic malignancy. Despite recent therapeutic advancements, the high relapse rate associated with extramedullary involvement remains a challenging issue. Moreover, therapeutic targets that regulate the extramedullary infiltration of AML cells are still not fully elucidated. The Aryl Hydrocarbon Receptor (AHR) is known to influence the progression and migration of solid tumors; however, its role in AML is largely unknown. This study explored the roles of AHR in the invasion and migration of AML cells. We found that suppressed expression of AHR target genes correlated with an elevated relapse rate in AML. Treatment with an AHR agonist on patient-derived AML cells significantly decreased genes associated with leukocyte trans-endothelial migration, cell adhesion, and regulation of the actin cytoskeleton. These results were further confirmed in THP-1 and U937 AML cell lines using AHR agonists (TCDD and FICZ) and inhibitors (SR1 and CH-223191). Treatment with AHR agonists significantly reduced Matrigel invasion, while inhibitors enhanced it, regardless of the Matrigel's stiffness. AHR agonists significantly reduced the migration rate and chemokinesis of both cell lines, but AHR inhibitors enhanced them. Finally, we found that the activity of AHR and the expression of NMIIA are negatively correlated. These findings suggest that AHR activity regulates the invasiveness and motility of AML cells, making AHR a potential therapeutic target for preventing extramedullary infiltration in AML. [ABSTRACT FROM AUTHOR]

Aim: Climate change has profound effects on species' distributions, and it is crucial to understand how well physiological limits correspond to distribution patterns to provide realistic estimations of future range shifts and/or extinctions. Seaweeds are foundation species of global coastal ecosystems, and sea surface temperature is a main predictor to explain their distributions and redistributions under global warming. We here test the hypothesis that, in contrast to other marine ectotherms, physiological knowledge of temperature niches is a weak predictor for seaweed distributions. Location: Global. Time Period: Present (1984–2019). Taxa: Seaweeds. Methods: We analysed the predictive power of physiological temperature limits to predict real‐world distributions in 126 globally distributed seaweed species with linear and generalized linear mixed models. Results: In 72% of the species, there was a difference of ≥|2|°C between the physiological and the realized thermal limits. Both, thermal underfilling (distributional thermal limits narrower than the physiological limits) and overfilling (distributional thermal limits wider than the physiological limits) were present. Thus, in only 28% of the species the physiological limits corresponded to the distributional limits. While heat‐tolerance is a significant predictor for upper distributional temperature limits, we found no relationship between cold‐tolerance and lower distributional temperature limits and the latter two seem to be independent. Main Conclusions: Physiological thermal limits have limited predictive power for seaweed distributions and deviations may be large. Especially cold‐tolerances are a weak predictor, and forecasting of migrations under changing global conditions (e.g. towards the poles) will need special attention. This indicates that responses towards climate change might be highly variable between seaweed species and difficult to predict. Further, nearly 60% of the investigated species had populations which are close to or beyond their reported upper survival limits and are thus probably under threat of eradication by elevation of sea surface temperature. [ABSTRACT FROM AUTHOR]

m6A demethylase FTO is confirmed to be involved in pancreatic cancer progression. FTO regulates miRNA processing. To investigate the regulatory effect of FTO on miR-383-5p and its role in pancreatic cancer. The expression of miR-383-5p, ITGA3, and FTO was predicted using bioinformatic analysis in tissues and was measured using qPCR in cells. Cell biological functions were investigated using MTT assay, Transwell assay, sphere formation assay, and qPCR. The targeting relationship between miR-383-5p and ITGA3 was evaluated using the dual-luciferase reporter assay. The effect of FTO on miR-383-5p processing was evaluated using RIP and MeRIP assay. FTO expression was upregulated in pancreatic cancer and silencing of FTO promoted the processing of miR-383-5p in an m6A-dependent manner. m6A-modified miRNA processing was recognized by IGF2BP1. Downregulation of miR-383-5p reversed FTO knockdown-induced inhibition of cellular processes. The FTO/miR-383-5p/ITGA3 axis facilitated cell viability, metastasis, and stemness in pancreatic cancer. [ABSTRACT FROM AUTHOR]

Riparian ecosystems are under a serious threat of invasion due to the clearance of riparian vegetation, which allows for increased light levels at ground level. This study presents the interactions between native Alternanthera sessilis (L.) R. Br. ex DC and invasive Alternanthera philoxeroides (Mart.) Griseb. during the colonization stage along a light gradient under tropical climate conditions. We conducted a 6 week growth experiment with monocultures of A. philoxeroides and A.sessilis and mixed communities of two species under four light levels (100%, 46%, 26% and 14% of full sunlight). Exposure to full sunlight (nearly 1800 μmol m−2 s−1) resulted in a significantly high biomass accrual in both species. However, biomass accrual did not correlate with the light intensity. At higher shade levels, reduction of lateral spread and shoot/root ratio was observed. Community composition had no influence on biomass accrual or morphological variations. Plasticity index values were approximately same in both species. Total relative yield was approximately two in all shade conditions, indicating that the two species interact neutrally along the light gradient. Therefore, the results of the study indicate that increased light levels will accelerate the proliferation of both species in riparian zones. Nevertheless, increased or decreased shade is unlikely to alter neutral interactions between A. philoxeroides and A. sessilis. [ABSTRACT FROM AUTHOR]

Glioblastomas are aggressive brain tumors for which effective therapy is still lacking, resulting in dismal survival rates. These tumors display significant phenotypic plasticity, harboring diverse cell populations ranging from tumor core cells to dispersed, highly invasive cells. Neuron navigator 3 (NAV3), a microtubule‐associated protein affecting microtubule growth and dynamics, is downregulated in various cancers, including glioblastoma, and has thus been considered a tumor suppressor. In this study, we challenge this designation and unveil distinct expression patterns of NAV3 across different invasion phenotypes. Using glioblastoma cell lines and patient‐derived glioma stem‐like cell cultures, we disclose an upregulation of NAV3 in invading glioblastoma cells, contrasting with its lower expression in cells residing in tumor spheroid cores. Furthermore, we establish an association between low and high NAV3 expression and the amoeboid and mesenchymal invasive phenotype, respectively, and demonstrate that overexpression of NAV3 directly stimulates glioblastoma invasive behavior in both 2D and 3D environments. Consistently, we observed increased NAV3 expression in cells migrating along blood vessels in mouse xenografts. Overall, our results shed light on the role of NAV3 in glioblastoma invasion, providing insights into this lethal aspect of glioblastoma behavior. [ABSTRACT FROM AUTHOR]

Backgrounds: Currently, family with sequence similarity 65 member A (FAM65A) is reported as a pivotal regulator in various cancers. However, the effect of FAM65A in lung squamous cell carcinoma (LSCC) is still unclear, the prime objective of this research is to explore the role of FAM65A in LSCC. Methods: Gene expression data and correlated clinical information were downloaded from the public database and the expression of FAM65A was detected. The expression of FAM65A was also detected in our collected clinical samples and LSCC cell lines. Survival package of R language was used to determine the survival significance of FAM65A. Proteins expression level was determined via western blot assay. Cell function experiments and in vivo experiments were performed to explore the effect of FAM65A on LSCC cell biological behaviors. Results: FAM65A expression was significantly increased in LSCC clinical samples and cell lines. High FAM65A expression predicted poor prognosis in LSCC patients. After silencing FAM65A, the ability of LSCC cell proliferation, invasion and migration was decreased, and LSCC cell cycle was blocked. Moreover, in vivo experiments revealed that silencing FAM65A could inhibit LSCC cell proliferation. Conclusions: High FAM65A expression could enhance proliferative, invasive and migratory abilities of LSCC. FAM65A might be a novel biomarker of LSCC. [ABSTRACT FROM AUTHOR]

Purpose: Uterine serous carcinoma (USC) is a highly aggressive and frequently recurring subtype of endometrial cancer with limited treatment options for advanced or recurrent stages. Sulindac, a classic non-steroidal anti-inflammatory drug, has demonstrated anti-tumor activity in several pre-clinical tumor models. This study aims to evaluate the effect of sulindac on cell proliferation and invasion in USC cells. Methods: Human USC cell lines ARK-1 and SPEC2 were treated with different concentrations of sulindac. Cell proliferation was assessed using MTT and colony formation assays. ELISA assays measured cellular stress, cleaved caspase 3 activity, antioxidant ability, and adhesion. Cell cycle arrest was evaluated by Cellometer. The invasive capability was detected by wound healing assay. Western blotting was used to analyze the changes in protein expression induced by sulindac. Results: Exposure to sulindac decreased cellular viability in a dose-dependent manner in ARK-1 and SPEC2 cells. Sulindac effectively inhibited cell cycle progression, increased cellular stress, caused apoptosis, and reduced cell adhesion and invasion in USC cells. Additionally, sulindac decreased the expression of COX-2 and blocked phosphorylation of NF-κB induced by TNF-α. Conclusion: Sulindac is a potential therapeutic agent for USC that deserves further exploration in pre-clinical studies and potentially future clinical trials. [ABSTRACT FROM AUTHOR]

Objective：To analyze the expression of malic enzyme 3 (ME3) in hepatocellular carcinoma (HCC) tissues and celllines, and explore the effects of ME3 on the proliferation, migration, and invasion of HCC cells, as well as its underlying mechanism. Methods：The Cancer Genome Atlas (TCGA) database was used to study the expression of ME3 in HCC tissues. RT - qPCR and Western blot were performed to detect the mRNA and protein expression levels of ME3 in HCC cells. After knocking down or over expressing ME3 in HCC cell lines, the effects of ME3 on the proliferation, migration and invasion of HCC cells were detected by CCK-8 assay, colony formation assay, transwell assay, and invasion assay. Western blot was used to detect the expression of proteins related to the PI3K/AKT signaling pathway. Results：Compared with adjacent normal tissues and normal liver celline, ME3 was significantly up-regulated in HCC tissues and cell lines. Knockdown of ME3 markedly inhibited the ability of proliferation, migration and invasion of HCC cells, while overexpression of ME3 resulted in the opposite effects. Furthermore, we found that the activity of PI3K/AKT signaling pathway was significantly activated by ME3. Conclusion：ME3 is highly expressed in HCC tissues, promoting the proliferation, migration and invasion of HCC cells, and may function as an oncogene in HCC by activating the PI3K/AKT signaling pathway． [ABSTRACT FROM AUTHOR]

Successful invasion of biological entities does not merely depend on the rigorous habitat attributes of invaded regions, besides, the intrinsic traits of the invader species also play a significant role in the process of invasion. Evaluation of plants' functioning across habitats helps in understanding which traits are contributing to invasion success in response to changing environmental factors as well as the habitat preference and vulnerability of invasive plants. This study analyzed the effects of forest types on the growth and reproduction capacity of a dreadful invasive alien weed Ageratina adenophora (Spreng.) King and Rob. Different forest types selected for the present study were Sal, Sal-mixed, Chir-Pine, Banj-Oak, Cypress, and Kharsu-Oak forests in Kumaun Himalaya, India. At each forest site, twenty-four 1 × 1 m size quadrats were randomly laid during the peak growth period of A. adenophora (mid-March–April). The numbers of A. adenophora individuals/quadrats were also counted to compute the density of this weed in each forest type. Three plants were chosen at random from each quadrat and uprooted carefully followed by their morphological and reproductive traits assessment in each forest type following standard methods. To check the variability in soil physicochemical properties, the soil was collected from the surface layer (0–15 cm depth) of each forest type in replicates of three using soil corer. Other environmental variables like aspect, elevation, and solar irradiance were also recorded for selected forest types. ANOVA results showed a significant effect of forest types on all the measured plant traits except root length (p = 0.427), root/shoot ratio (p = 0.201), and root weight ratio (p = 0.225). Soil physicochemical properties also showed considerable variations across forest types except for soil pH. The maximum density (109 individuals/m2), plant height, (149.6 cm/plant), aboveground biomass (19.59 g/plant), and belowground biomass (2.82 g/plant) were recorded in the Cypress forest population, while the lowest growth was recorded in the Kharsu-Oak forest population with 10 individuals/m2 density, 57.94 cm plant height, 3.36 g aboveground biomass, and 0.30 g belowground biomass/plant. Generally, A. adenophora allocated maximum biomass to shoots (57–81%), thus increasing carbon assimilation, while minimum biomass was allocated to reproductive parts (0–17%) indicating higher growth through vegetative propagation. Leaf area was highest in the Banj-Oak forest (2266.04 cm2), while reproductive performance in terms of seed numbers (13,646 seeds/plant), seed weight (0.54 g/plant), and reproductive index (119.26) was highest in the Sal-mixed forest. This study concluded that A. adenophora acclimates to heterogeneous environments in different forest ecosystems through higher plasticity in most of the observed traits. The maximum growth performance of A. adenophora recorded in open-canopied Cypress forest suggested some kind of shade treatment before the emergence of the invader as a control measure to check the invasion. [ABSTRACT FROM AUTHOR]

Islands harbor a significant proportion of global biodiversity and also have disproportionately high richness of introduced species relative to continents. Given the sensitivity of island ecosystems to introduced species, data deficiencies on introduction pathways, patterns of establishment, and potential impacts of introduced species can hamper mitigation and conservation efforts on islands. The Caribbean region is emerging as a hotspot for introduced amphibian and reptile (herpetofaunal) species, but patterns associated with herpetofaunal introductions on specific islands are not well explored. Here, we perform a detailed investigation of Aruba, a small Caribbean island with an exceptionally high number of introduced herpetofaunal species. We compile a database from the literature of introduction pathways, introduction years, source locations, native ranges, establishment outcomes, habitat use, and ecological impacts for three newly documented species and the 12 previously documented introduced herpetofaunal species on Aruba. From this database we synthesize emergent introduction patterns on Aruba and highlight areas of data deficiency. Overall, the patterns on Aruba echo the patterns exhibited in the greater Caribbean region. Introduction rates on Aruba have been increasing exponentially, yet the introduction pathways and source locations of most species are unknown. Following introduction, most species successfully establish localized populations in anthropogenic habitat, but the ecological impacts of most species have not been well-assessed. We suggest increased monitoring of shipments will help identify potential pathways to slow the introduction of new species, and further studies of ecological impacts of introduced species are needed. [ABSTRACT FROM AUTHOR]

Cycads hold important economic and conservation value. Some species are extensively used in landscaping, while others are endangered and legally protected. The Australian cycad-attacking weevil, Siraton internatus, is notably destructive, occasionally causing infestations and invasions across various countries. This study simulated habitat suitability for S. internatus to assess its potential invasion and the impact of climate change. Habitat suitability was evaluated under current climate and four climate change scenarios over two time frames (2050 and 2090). Furthermore, we investigated the threat posed by S. internatus to cycad reserves, using Taiwanese reserves as a representative case. Our MaxEnt predictions demonstrated high accuracy, meeting multiple evaluation criteria. We explored the potential distribution of S. internatus within Australia and internationally, identifying suitable habitats in Africa, the Americas, Asia, and Europe. The case study highlighted the low habitat suitability within the two Taiwanese cycad reserves, which is projected to decrease to unsuitable levels under future climate change scenarios for this weevil species. Moreover, our results revealed that suitable habitat for S. internatus is projected to contract globally under all climate scenarios and time periods, but expansion in Chile and the southern Himalaya (e.g., Nepal). This study provides valuable insights into cycad conservation and pest invasion risks. The results support both global and local efforts to manage the invasion threats from this destructive Australian cycad-attacking weevil species. It also accentuates the urgency for continuous biosecurity inspections and prevention of exporting mature cycad caudexes from Australia. [ABSTRACT FROM AUTHOR]

Many theories have been created to explain the mechanisms driving species coexistence. They are mainly based on biotic interactions and abiotic factors, which are being constantly affected by human activities. In invaded communities, novel ecological interactions among organisms are created and native and non-native species have to coexist. This coexistence can be supported by different interactions (both positive and negative) and, in some cases, can be followed by negative impacts on the spatial distribution of native species. We aimed to assess the role of the functional differences and species status influencing co-occurrence patterns between native and non-native species at the Upper Paraná River floodplain, Southern Brazil. We estimated the co-occurrence between pairs of native and non-native species and their functional dissimilarity using morphological traits. We found a positive relationship between co-occurrence and functional dissimilarity between species: more similar native and non-native species tended to co-occur less. The co-occurrence was also related to species status: it was higher between pairs of native species than between pairs of native and non-native species. Niche differentiation may play an important role in driving the observed co-occurrence patterns at small spatial scales. However, this can lead to a limitation on the space use of species and modifications in the taxonomic and functional diversity of the native community. Although we recognize that species coexistence may be driven by several factors, we show here that the co-occurrence patterns of native and non-native species were affected by their functional dissimilarity. [ABSTRACT FROM AUTHOR]

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In order to investigate the effects of RNAi-mediated survivin and hypoxia-inducible factor 1α (HIF-1α) gene silencing on the proliferation and apoptosis of gastric cancer BGC-823 cells, small interfering RNAs (siRNAs) targeting survivin and HIF-1α mRNAs, respectively, as well as scrambled siRNAs (SCRs) were designed and synthesized, namely siRNA-survivin group, siRNA-HIF-1α group, and SCR group. The hypoxia-sensitive gastric cancer BGC-823 cells were identified and transfected in vitro with Hifectin II under hypoxic conditions, and the expression of survivin and HIF-1α was assessed by RT-PCR and Western blotting assays, respectively. The ability of apoptosis, proliferation, invasion, and migration was measured, and the results showed that HIF-1α expression was significantly increased in BGC-823 cells under hypoxic conditions, and survival-targeted siRNA transfection decreased the expression of survivin under hypoxic conditions, while co-transfection of survivin-targeted siRNA and HIF-1α-targeted siRNA down-regulated both survivin and HIF-1α expression. Compared with the blank control group, the co-transfected siRNA group exhibited distinct characteristics, with decreased invasion and migration ability, increased apoptosis, and significantly decreased cell proliferation under hypoxic conditions. It was confirmed that the downregulation of survivin and HIF-1α in BGC-823 cells may induce anticancer effects by enhancing apoptosis and decreasing proliferation, migration, and invasion ability. The novelty lies in the application of RNAi technology to silence the expression of both survivin and HIF-1α genes in gastric cancer BGC-823 cells by single and combined interference in an established gastric cancer cell model and observed the mechanism of its effect on the proliferation and apoptosis of gastric cancer cells. Concerning the success of this highly active antiretroviral therapy of gene disruption therapies, which is the first of its kind in the world, we wonder whether we can find other better gene targets for more kinds of tumor therapy. [ABSTRACT FROM AUTHOR]

High mortality rate of melanoma is due to the metastasis of malignant cells. Galbanic acid (GBA) is a natural sesquiterpene coumarin with valuable pharmaceutical activities. Our study aimed to investigate whether GBA can affect the migration, invasion, and adhesion of melanoma cells. The survival rate of B16F10 cells was measured using the alamarBlue assay. Scratch, adhesion, and invasion assays were performed to determine the effect of GBA on metastatic behavior of cells. Moreover, gelatin zymography was done to assess the activity of MMP-2 and MMP-9, and qRT-PCR was used to investigate the effect of GBA on the expression of candidate genes. Based on the results of alamarBlue assay, 40 µM GBA was chosen as the optimum concentration for all tests. Our findings indicated that GBA significantly decreased the invasion and migration of B16F10 cells while enhancing their adhesion ability. In addition, gelatin zymography demonstrated that GBA reduced the enzymatic activity of MMP-2 and MMP-9. Moreover, qRT-PCR revealed that GBA reduced the expression of N-cadherin and fibronectin. Current findings demonstrated, for the first time, that GBA inhibited the migration and invasion of melanoma cells via reducing the activity of MMP-2 and MMP-9 and downregulating N-cadherin and fibronectin expression. Accordingly, GBA could be suggested as a potential therapeutic agent for the treatment of melanoma. [ABSTRACT FROM AUTHOR]

Phragmites australis is one of the most invasive wetland plants on the planet with both native and invasive haplotypes occurring in the United States. Three Phragmites haplotypes (Delta-, EU- and Gulf-types) co-occur in marshes of the Mississippi River Delta (MRD), where a recent dieback of Phragmites has prompted investigations about the potential for recolonization by seed. In other areas of the US, the invasive EU-type has been shown to spread by seed, yet little is known about reproduction modes of the Delta- and Gulf-types. We conducted a survey at 35 sites along the Mississippi River Delta region in southeast Louisiana to examine the potential for sexual reproduction across haplotypes as well as the potential for hybridization. Seed and pollen samples were collected from Phragmites populations to examine flowering phenology and determine pollen viability of the three lineages. We also conducted a seedbank assay in stands of three haplotypes to test the potential for recruitment by seed. Despite the observed potential for sexual reproduction in Delta- and EU- types, no Phragmites seedlings germinated from the seedbank. EU was the only haplotype to exhibit germination from seeds collected from seed heads. Both spatial separation and temporal isolation in flowering times indicate that hybridization between Phragmites haplotypes in the lower MRD is unlikely. High pollen production, increased pollen production following dieback, and viable seeds in the EU-type suggest that this invasive haplotype has a greater potential to invade new areas and adapt to stressors through sexual reproduction compared to than Delta-or Gulf haplotypes. [ABSTRACT FROM AUTHOR]

Background: Renal cell carcinoma (RCC) is presently recognized as the most prevalent kidney tumor. However, the role and underlying mechanism of action of the conversion factor-inducible protein (TGFBI), an extracellular matrix protein, in RCC remain poorly understood. Methods: In this study, we employed Western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and immunohistochemistry techniques to assess the expression of TGFBI in RCC tissues or cells. Furthermore, we analyzed the proliferation and migration of RCC cells using CCK8, cloning, scratching, and migration assays. Additionally, we examined apoptosis and cell cycle progression through flow cytometry, analysis. Lastly, we employed gene set enrichment analysis (GSEA) to investigate the biological processes associated with TGFBI, which were subsequently validated. Results: The findings indicate that TGFBI exhibits significantly elevated expression levels in both renal cell carcinoma (RCC) tissues and cells. Furthermore, the knockdown of TGFBI in SiRNA transfected cells resulted in the inhibition of RCC cell proliferation, migration, invasiveness, apoptosis, and alteration of the cell cycle. Additionally, TGFBI was found to impede the epithelial-mesenchymal transition (EMT) process in RCC cells. Bioinformatics analysis suggests that TGFBI may exert its influence on various biological processes in RCC through the tumor immune microenvironment. Moreover, our study demonstrates that TGFBI promotes RCC progression by activating the PI3K/AKT/mTOR/HIF-1α. Conclusions: Our research indicates that TGFBI exhibits high expression in RCC and facilitate RCC progression and metastasis through various molecular mechanisms. Hence, TGFBI has the potential to be a novel therapeutic target for the diagnosis and treatment of RCC in the future. [ABSTRACT FROM AUTHOR]

The epithelial–mesenchymal transition (EMT) is a genetic reprogramming that tumor cells utilize for metastasis. Epsin-3 (EPN3) is an endocytic adapter protein involved in clathrin-mediated endocytosis and had been previously linked to EMT in breast cancer and glioma metastasis. In this study, identified the role of epsin-3 in lung adenocarcinoma and metastasis and epsin-3 levels identified using an expression profile analysis of patient data indicated the protein was abnormally overexpressed in lung adenocarcinoma patients and this was directly linked to disease severity. Gene knockdowns of EPN3 in human adenocarcinoma cell line A549 and the non-small cell lung carcinoma cell line H1299 decreased the levels of mesenchymal markers, including vimentin (VIM), N-cadherin (NCAD) and embryonic transcription factors like zinc finger E-box binding homeobox 1(ZEB1), snail, and the key molecules of Wnt pathway such as β-catenin and resulted in increased expression of the epithelial marker E-cadherin (ECAD). Our data links EPN3 to the EMT process in lung cancer and inhibition of its expression reduced the metastatic and invasive ability of lung adenocarcinoma cells by inhibiting the EMT process. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have emerged as important players in cancer progression. Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer with increasing incidence worldwide. The prognosis of the metastatic cSCC is poor, and currently there are no established biomarkers to predict metastasis risk or specific therapeutic targets for advanced or metastatic cSCC. To elucidate the role of lncRNAs in cSCC, RNA sequencing of patient derived cSCC cell lines and normal human epidermal keratinocytes was performed. The correlation analysis of differentially expressed lncRNAs and protein-coding genes revealed six distinct gene clusters with one of the upregulated clusters featuring genes associated with cell motility. Upregulation of the expression of lncRNAs linked to cSCC cell motility in cSCC and head and neck SCC (HNSCC) cells was confirmed using qRT-PCR. Elevated expression of HOTTIP and LINC00543 was also noted in SCC tumors in vivo and was associated with poorer prognosis in HNSCC and lung SCC cohorts within TCGA data, respectively. Altogether, these findings uncover a novel set of lncRNAs implicated in cSCC cell locomotion. These lncRNAs may serve as potential novel biomarkers and as putative therapeutic targets for locally advanced and metastatic cSCC. [ABSTRACT FROM AUTHOR]

The Croaking Gourami Trichopsis vittata (Cuvier, 1831) is a native fish to southeastern Asia and Sundaland, with introduction reports from the USA, Philippines, and many other countries including India. In India, this species was first reported from Chembarampakkam Lake situated in Chennai during the year 2015. This study reports the presence of this fish for the first time in the Magra Beel, a wetland in the district of Nadia, West Bengal, in 2021, 2022, 2023. The laboratory evaluated the fish samples taken from the marsh to determine their fin ray counts and morphometric data. The results identified the species as T. vittata and supported previous research. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the effects and the related signaling pathway of miR-362-3p on OS. Methods: The bioinformatics analysis approaches were employed to investigate the target pathway of miR-362-3p. After the 143B and U2OS cells and nu/nu male mice were randomly divided into blank control (BC) group, normal control (NC) group, and overexpression group (OG), the CCK-8, EdU staining, wound healing assay, Transwell assay, and TUNEL staining were adopted to respectively determine the effects of overexpressed miR-362-3p on the cell viability, proliferation, migration, invasion, and apoptosis of 143B and U2OS cells in vitro, tumor area assay and hematoxylin and eosin staining were employed to respectively determine the effects of overexpressed miR-362-3p on the growth and pathological injury of OS tissue in vivo. The qRT-PCR, Western blot, and immunohistochemical staining were applied to respectively investigate the effects of overexpressed miR-362-3p on the IL6ST/JAK2/STAT3 pathway in OS in vivo and in vitro. Results: The bioinformatics analysis approaches combined qRT-PCR indicated that the IL6ST/JAK2/STAT3 is one of the target pathways of miR-362-3p. Compared with NC, the cell viability, proliferation, migration, and invasion of 143B and U2OS cells were dramatically (P < 0.01) inhibited but the apoptosis was prominently (P <0.0001) promoted in OG. Compared with NC, the growth of OS tissue was significantly (P < 0.05) suppressed and the pathological injury of OS tissue was substantially aggravated in OG. The gene expression levels of IL6ST, JAK2, and STAT3 and the protein expression levels of IL6ST, JAK2, p-JAK2, STAT3, and p-STAT3 in 143B and U2OS cells were memorably (P < 0.0001) lower in OG than those in NC. In addition, the positively stained areas of proteins of IL6ST, JAK2, p-JAK2, STAT3, and p-STAT3 of OS tissue in OG were markedly (P < 0.01) reduced compared with those in NC. Conclusion: The overexpression of miR362-3p alleviates OS by inhibiting the IL6ST/JAK2/STAT3 pathway in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Osteosarcoma is an aggressive form of bone cancer and affects the health in children and adolescents. Although conventional treatment improves the osteosarcoma survival, some patients have metastasis and drug resistance, leading to a worse prognosis. Therefore, it is necessary to explore the molecular mechanism of osteosarcoma occurrence and progression, which could discover the novel treatment for osteosarcoma. Long noncoding RNAs (lncRNAs) have been reported to regulate osteosarcoma occurrence and malignant progression. LncRNA HOXA-AS3 facilitates the tumorigenesis and progression in a variety of human cancers. However, the underlying mechanism of lncRNA HOXA-AS3-induced oncogenesis is poorly determined in osteosarcoma. To address this point, we utilized several cellular biological strategies and molecular approaches to explore the biological functions and mechanisms of lncRNA HOXA-AS3 in osteosarcoma cells. We found that lncRNA HOXA-AS3 facilitates cell proliferation and invasion via targeting miR-218-5p/FOXP1 axis in osteosarcoma. In conclusion, lncRNA HOXA-AS3 could be a promising target for osteosarcoma treatment. [ABSTRACT FROM AUTHOR]

Context: There is mounting evidence implicating kisspeptin signalling in placental development and function. Aims: This study aimed to elucidate kisspeptin's role in trophoblast invasion and migration using three experimental models. Methods: First, we examined the mouse fetus and placenta in a kisspeptin receptor (Kiss1r) knockout (KO) model. Fetal/placental weights and gene expression (quantitative polymerase chain reaction) were assessed. Second, we determined kisspeptin effects on a human trophoblast (BeWo) cell line in vitro. Third, we examined KISS1 and KISS1R gene expression in human placenta from term and pre-term pregnancies. Key results: No difference was found in fetal or placental weight between Kiss1r KO and wildtype mice. However, expression of the trophoblast invasion marker, Mmp2 mRNA, was greater in the placental labyrinth zone of Kiss1r KO mice. BeWo cell models of villus cytotrophoblast and syncytiotrophoblast cells exhibited kisspeptin protein expression, with greater expression in syncytiotrophoblast, consistent with KISS1 mRNA. Kisspeptin treatment inhibited the migratory potential of cytotrophoblast-like cells. Finally, while no difference was seen in KISS1 and KISS1R mRNA between term and pre-term placentas, we saw a difference in the relative expression of each gene pre-term. We also observed a positive correlation between KISS1 expression and maternal body mass index. Conclusions: Our results indicate that kisspeptin may inhibit trophoblast invasion. Implications: Further investigation is required to clarify specific regulatory mechanisms. There is mounting evidence implicating kisspeptin signalling in placental development and function. We sought to elucidate kisspeptin's role in the placenta using three experimental models: a mouse kisspeptin receptor knockout model, culture of human BeWo trophoblast cells, and a human placenta punch biopsy. Our results indicate that kisspeptin may inhibit trophoblast invasion, although further investigation is required to clarify specific regulatory mechanisms. Image by and adapted from M. Arvola and R. Mattsson (). [ABSTRACT FROM AUTHOR]

Recent studies have revealed that long non-coding RNAs (IncRNAs) involve in the progression of oral squamous cell carcinoma (OSCC). These IncRNAs have emerged as biomarkers or therapeutic targets for OSCC. We here aimed to investigate the role of IncRNA LINC01315 in OSCC and the related mechanisms. LINC01315 and DLG3 were determined to be poorly expressed while microRNA-211 (miR-211) was highly expressed in OSCC tissues and cells using RT-qPCR and western blot analysis. Based on the results obtained from dual-luciferase reporter gene, RIP, and FISH assays, LINC01315 was found to upregulate DLG3 expression by competitively binding ETRAC to miR-211. Upon altering the expression of LINC01315, and/or miR-211 in OSCC cells with shRNA, mimic, or an inhibitor, we assessed their effects on OSCC cell proliferation, migration, invasion, and apoptosis. LINC01315 knockdown enhanced OSCC cell proliferation, migration and invasion, but dampened their apoptosis, all of which could be reversed by miR-211 inhibition. Elevation of DLG3, a target gene of miR- 211, activated the Hippo signaling pathway, whereby suppressing OSCC progression in vitro. Finally, their roles in tumor growth were validated in vivo. These findings suggest that LINC01315 elevates DLG3 expression by competitively binding to miR-211, thereby suppressing OSCC progression. [ABSTRACT FROM AUTHOR]

Breast cancer is a diverse illness that originates from genetically modified cells in the mammary epithelium. It is characterized by complex interactions between the tumor cells and the surrounding tumor microenvironment (TME). This study examines the signaling pathways of integrins in mammary epithelial cells and mammary neoplasia by doing a thorough analysis of the current literature. Integrins are transmembrane receptors that facilitate cellular interactions with extracellular matrix (ECM) proteins, including laminin, fibronectin, and collagen. They are composed of a and ß subunits that combine to create heterodimers. These interactions play a vital role in the process of cell adhesion, migration, survival, and the maintenance of tissue integrity. The signaling pathways of Integrin-ECM, which involve focal adhesion complexes and kinases such as FAK and Src, govern cellular processes such as proliferation, differentiation, and survival. Integrins play a crucial role in the creation and upkeep of the ductal tree and alveoli during mammary gland development, which are necessary for lactation. Altered expression and signaling of integrins in breast neoplasia contribute to the advancement, invasion, and spread of tumors. Integrins participate in two-way communication, influencing the behavior of cancer cells and their interactions with the tumor microenvironment (TME), which consists of stromal and immune cells. Integrins such as avß3 and a6ß4 have important functions in cell migration, the formation of new blood vessels, and the survival of cancer cells." Comprehending the dual function of integrin signaling in both promoting and inhibiting tumors is essential for the development of precise cancer treatments. Integrin-based therapies show potential for altering these pathways, thereby enhancing cancer outcomes by suppressing tumor growth and spread. Subsequent investigations should prioritize the comprehensive examination of the regulatory mechanisms governing integrins and their potential as targets for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Elodea nuttallii represents non-native and highly invasive species in Europe that significantly influence freshwater plant communities by decreasing the diversity of native species. This study aimed to determine whether the morphological and anatomical features of Potamogeton gramineus, a native species in Vlasina Lake, differ between sites where it coexists with E. nuttallii and those where E. nuttallii is not present. Environmental variables such as water depth, temperature, pH, conductivity, saturation, and O2 concentration were included in the analysis. Analyses were conducted on 32 morphological and anatomical features of P. gramineus collected from six sites within Vlasina Lake, comprising three sites where E. nuttallii was present and three sites where it was absent. The datasets containing morphometric and environmental variables underwent analysis using standard univariate techniques (Descriptive, ANOVA), Tukey's Honest Significant Difference (HSD) test, Student's t-test, and the Mann–Whitney U test, as well as multivariate statistical methods such as Canonical Discriminant Analysis (CDA). The results show the presence of morphological differentiation among P. gramineus individuals across the analyzed sites. These findings suggest that morphological and anatomical features, such as epidermis, mesophyll, palisade, and aerenchyma tissue thickness in floating leaves, number, length, width, and the surface area of stomata, as well as the width of submersed leaves and stem aerenchyma tissue thickness, effectively differentiate individuals that coexist with E. nuttallii and individuals that growth without its presence. Moreover, they indicate that P. gramineus exhibits a notable ability to modify its morphological traits in response to invasion. [ABSTRACT FROM AUTHOR]

Iron death is considered to be an iron-dependent, non-apoptotic form of regulated cell death, which is mainly triggered by reactive oxygen species (ROS) production and imbalance of iron homeostasis leading to severe lipid peroxidation, and it induces related factors that can directly or indirectly affect glutathione peroxidase through different pathways, leading to decreased antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in the cells, and ultimately leading to oxidative cell death. Meanwhile, iron death is regulated by various pathways, such as iron metabolism, mitochondrial activity, redox homeostasis, and disease-related signalling pathways. It has been reported that dysregulation of iron death metabolic pathways can affect the development and progression of hepatocellular carcinoma. Little is known about the molecular mechanisms by which iron death leads to disease, but iron death-related genes and pathways are associated with hepatocellular carcinoma progression. It was found that abnormal activation of the Wnt/β-catenin signalling pathway is associated with recurrence, invasion, metastasis and immune escape of hepatocellular carcinoma, and is closely linked to iron death. This pathway can further aggravate the progression of hepatocellular carcinoma by regulating the occurrence of iron death. Some substantial progress has been made in this field in hepatocellular carcinoma. Therefore, in the present review, we will explore the process of iron death by outlining its molecular mechanism and its role in hepatocellular carcinoma, and at the same time, we will specifically analyse the Wnt/β-catenin signaling pathway to regulate the process of iron death, so as to provide a reliable scientific theoretical basis for the treatment of hepatocellular carcinoma in the future. [ABSTRACT FROM AUTHOR]

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Background: The Aedes albopictus mosquito is of medical concern due to its ability to transmit viral diseases, such as dengue and chikungunya. Aedes albopictus originated in Asia and is now present on all continents, with the exception of Antarctica. In Mozambique, Ae. albopictus was first reported in 2015 within the capital city of Maputo, and by 2019, it had become established in the surrounding area. It was suspected that the mosquito population originated in Madagascar or islands of the Western Indian Ocean (IWIO). The aim of this study was to determine its origin. Given the risk of spreading insecticide resistance, we also examined relevant mutations in the voltage-sensitive sodium channel (VSSC). Methods: Eggs of Ae. albopictus were collected in Matola-Rio, a municipality adjacent to Maputo, and reared to adults in the laboratory. Cytochrome c oxidase subunit I (COI) sequences and microsatellite loci were analyzed to estimate origins. The presence of knockdown resistance (kdr) mutations within domain II and III of the VSSC were examined using Sanger sequencing. Results: The COI network analysis denied the hypothesis that the Ae. albopictus population originated in Madagascar or IWIO; rather both the COI network and microsatellites analyses showed that the population was genetically similar to those in continental Southeast Asia and Hangzhou, China. Sanger sequencing determined the presence of the F1534C knockdown mutation, which is widely distributed among Asian populations, with a high allele frequency (46%). Conclusions: These results do not support the hypothesis that the Mozambique Ae. albopictus population originated in Madagascar or IWIO. Instead, they suggest that the origin is continental Southeast Asia or a coastal town in China. [ABSTRACT FROM AUTHOR]

Background: Breast cancer has become a major public health problem in the current society, and its incidence rate ranks the first among Chinese female malignant tumors. This paper once again confirmed the efficacy of lncRNA in tumor regulation by introducing the mechanism of the diagnosis of breast cancer by the MIR497HG/miR-16-5p axis. Methods: The abnormal expression of MIR497HG in breast cancer was determined by RT-qPCR method, and the correlation between MIR497HG expression and clinicopathological characteristics of breast cancer patients was analyzed via Chi-square test. To understand the diagnostic potential of MIR497HG in breast cancer by drawing the receiver operating characteristic curve (ROC). The overexpressed MIR497HG (pcDNA3.1-MIR497HG) was designed and constructed to explore the regulation of elevated MIR497HG on biological function of BT549 and Hs 578T cells through Transwell assays. Additionally, the luciferase gene reporter assay and Pearson analysis evaluated the targeting relationship of MIR497HG to miR-16-5p. Results: MIR497HG was decreased in breast cancer and had high diagnostic function, while elevated MIR497HG inhibited the migration and invasion of BT549 and Hs 578T cells. In terms of functional mechanism, miR-16-5p was the target of MIR497HG, and MIR497HG reversely regulated the miR-16-5p. miR-16-5p mimic reversed the effects of upregulated MIR497HG on cell biological function. Conclusions: In general, MIR497HG was decreased in breast cancer, and the MIR497HG/miR-16-5p axis regulated breast cancer tumorigenesis, providing effective insights for the diagnosis of patients. [ABSTRACT FROM AUTHOR]

Insects are intentionally introduced to various regions out of their native ranges to perform fundamental functions, such as pest control, and some keep dispersing from introduction sites to become cosmopolitan and even invasive. The African horned dung beetle, Euoniticellus intermedius (Reiche) (Coleoptera: Scarabaeidae), has been intentionally introduced on multiple continents to bury cattle dung and control livestock pests, but has naturally dispersed and became very abundant at various latitudes and elevations out of its native and original introduction ranges. This beetle has been considered invasive, but there is no direct evidence of its effects on displacing native species. As it is highly fecund, E. intermedius has been an important model in experimental studies performed in nature and in the laboratory in multiple fields. In evolutionary biology, it serves as a model for sexual selection, given the sexual dimorphism characterized by the presence of a horn in males which is correlated with individual condition and strength, and which is absent in females. In ecotoxicology, it has been studied regarding physiological mechanisms of responses to contaminants, population declines, and evolutionary responses to challenging toxic conditions. Given its importance in burying dung in cattle pastures, experiments have also determined environmental conditions that limit this ecological function. Despite being unique in its tolerance to a wide variety of stressors and environments, this species is sensitive to current conditions of global change, including warming and pollution. We identify the most promising questions to be solved in physiology, ecology, and evolution, for which E. intermedius would be an ideal study system. [ABSTRACT FROM AUTHOR]

Many pathways of invasion have been posited, but ecologists lack an experimental framework to identify which mechanisms are dominant in a given invasion scenario. Plant–soil feedbacks (PSFs) are one such mechanism that tend to initially facilitate, but over time attenuate, invasive species' impacts on plant diversity and ecosystem function. PSFs are typically measured under greenhouse conditions and are often assumed to have significant effects under field conditions that change over time. However, direct tests of PSFs effects in natural settings and their change over time are rare. Here we compare the role of PSFs with the effects of biomass in limiting the dominance of an invasive species and impacts on resident species diversity. We characterized the effects of the invader Bromus inermis (Leyss.) on native plant communities over time and measured changes in its conspecific PSFs and vegetative growth to understand their integrated effects on community diversity. To do so, we combined data from a 6‐year field study documenting the rate and impacts of invasion with a short‐term greenhouse experiment quantifying PSF as a function of time since invasion in the field. We found that the nature and strength of B. inermis PSFs did not change over time and were not mediated by soil microbial communities. Though PSFs impacted B. inermis reproduction, they did not sufficiently limit vegetative growth to diminish the negative impacts of B. inermis biomass on native species. B. inermis experienced the full strength of its negative PSFs immediately upon invasion, but they were ineffective at reducing B. inermis vigor to facilitate the recovery of the native plant community. We recommend that conservation efforts focus on limiting B. inermis vegetative growth to facilitate community recovery. [ABSTRACT FROM AUTHOR]

Proline 4-hydroxylase 2 (P4HA2) is known for its hydroxylase activity, primarily involved in hydroxylating collagen precursors and promoting collagen cross-linking under physiological conditions. Although its overexpression influences a wide variety of malignant tumors' occurrence and development, its specific effects and mechanisms in oral squamous cell carcinoma (OSCC) remain unclear. This study focused on investigating the expression patterns, carcinogenic functions, and underlying mechanisms of P4HA2 in OSCC cells. Various databases, including TCGA, TIMER, UALCAN, GEPIA, and K-M plotter, along with paraffin-embedded samples, were used to ascertain P4HA2 expression in cancer and its correlation with clinicopathological features. P4HA2 knockdown and overexpression cell models were developed to assess its oncogenic roles and mechanisms. The results indicated that P4HA2 was overexpressed in OSCC and inversely correlated with patient survival. Knockdown of P4HA2 suppressed invasion, migration, and proliferation of OSCC cells both in vitro and in vivo, whereas overexpression of P4HA2 had the opposite effects. Mechanistically, the phosphorylation levels of the PI3K/AKT pathway were reduced following P4HA2 silencing. The study reveals that P4HA2 acts as a promising biomarker for predicting prognosis in OSCC and significantly affects metastasis, invasion, and proliferation of OSCC cells through the regulation of the PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Aims: We aimed to assess the oncological impact of micrometric extent of invasion in patients with pT1 bladder cancer (BCa) who underwent en‐bloc resection for bladder tumour (ERBT). Methods and results: We retrospectively analysed the records and specimens of 106 pT1 high‐grade BCa patients who underwent ERBT. The extent of invasion, such as depth from basal membrane, number of invasive foci, maximum width of invasive focus, muscularis mucosae invasion and infiltration pattern (pattern A: solid sheet‐like, nodular or nested growth, pattern B: trabecular, small cluster or single‐cell pattern) were evaluated by a single genitourinary pathologist. The end‐points were recurrence‐free (RFS) and progression‐free survival (PFS). Within a median follow‐up of 23 months, overall, 36 patients experienced recurrence and 13 patients experienced disease progression. The 2‐year PFS differed significantly depending on depth from basal membrane (< 1.3 mm: 94.8% versus ≧ 1.3 mm: 65.2%, P = 0.005), maximum width of invasive focus (< 4 mm: 91.7% versus ≧ 4 mm: 62.3%, P < 0.001), muscularis mucosae (MM) invasion (above MM = 96.1% versus into or beyond MM = 64.8%, P = 0.002) and infiltration pattern (pattern A: 100% versus pattern B: 83.3%, P = 0.037). In a multivariable analysis, MM invasion [hazard ratio (HR) = 4.54, 95% confidence interval (CI) = 1.25–16.5] and maximum width of invasive focus ≧ 4 mm (HR = 4.79, 95% CI = 1.25–16.5) were independent prognostic factors of progression. Conclusions: En‐bloc resection facilitates the evaluation of pathologic variables that might be useful in predicting disease recurrence and progression. In particular, not only the MM invasion but also the maximum width of invasion focus, reflecting the invasive volume, appear to be reliable prognosticators for disease progression. [ABSTRACT FROM AUTHOR]

The deliberate release of captive‐bred individuals, the accidental escape of domesticated strains, or the invasion of closely related conspecifics into wild populations can all lead to introgressive hybridization, which poses a challenge for conservation and wildlife management. Rates of introgression and the magnitude of associated demographic impacts vary widely across ecological contexts. However, the reasons for this variation remain poorly understood. One rarely considered phenomenon in this context is soft selection, wherein relative trait values determine success in intraspecific competition for a limiting resource. Here we develop an eco‐genetic model explicitly focussed on understanding the influence of such competitive interactions on the eco‐evolutionary dynamics of wild populations experiencing an influx of foreign/domesticated individuals. The model is applicable to any taxon that experiences natural or human‐mediated inputs of locally maladapted genotypes ('intrusion'), in addition to phenotype‐dependent competition for a limiting resource (e.g. breeding sites, feeding territories). The effects of both acute and chronic intrusion depended strongly on the relative competitiveness of intruders versus locals. When intruders were competitively inferior, density‐dependent regulation limited their reproductive success (ability to compete for limited spawning sites), which prevented strong introgression or population declines from occurring. In contrast, when intruders were competitively superior, this amplified introgression and led to increased maladaptation of the admixed population. This had negative consequences for population size and population viability. The results were sensitive to the intrusion level, the magnitude of reproductive excess, trait heritability and the extent to which intruders were maladapted relative to locals. Our findings draw attention to under‐appreciated interactions between phenotype‐dependent competitive interactions and maladaptive hybridization, which may be critical to determining the impact captive breeding programmes and domesticated escapees can have on otherwise self‐sustaining wild populations. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of inhibiting the expression of RNA component of mitochondrial RNA processing endoribonuclease(RMRP) on the proliferation and invasion of human lung cancer cell line A549 in order to provide evidence to support the research on NSCLC mechanism. Methods A total of 122 cases of patients who underwent surgical treatment were selected in Jiaozuo People's Hospital from March 2016 to March 2021. In the same period, 50 healthy people from physical examination center were selected as the control group. RT-qPCR was used to detect the expressions of RMRP in blood and tissues. Human lung cancer cell line A549 was cultured and divided into si-RMRP group, siRNA-NC group and blank group. RT-qPCR, CCK-8 and Transwell assays were used to detect the expression of RMRP, proliferation activity and cell counting of invasive cells. Results The rel- ative expression level of RMRP in the blood of NSCLC patients was significantly higher than that of control group (P < 0.001) The relative expression level of RMRP in NSCLC tissues was significantly higher than the adjacent tissues (P<0.001). The relative expression level of RMRP in blood and tissues of patients with poorly differenti- ated, lymph node metastasis and TNM stage III compared with moderate to highly differentiated, no lymph node metastasis and TNM stage III were significantly increased (P < 0.05) The relative expression level of RMRP in the cells of the si-RMRP group was lower than that of blank and the siRNA-NC group (P < 0.001) . Compared with the blank group and the siRNA-NC group, the absorbance (A) value of cells at 24, 48, 72 and 96 h in the siRMRP -group was decreased (P < 0.05) The number of invasion cells in the si-RMRP group was lower than that in the blank group and the siRNA-NC group (F = 27.765) P < 0.001 ) . Conclusions The relative expression levels of RMRP in blood and tissues of NSCLC patients are increased. Down-regulation of the expres- sion of RMRP gene in A549 cells can inhibit cell proliferation and reduce cell invasion. [ABSTRACT FROM AUTHOR]

Summary: The genus Oscheius includes species with different habits and some of them have been shown to kill some insect pests. The occurrence of Oscheius in hay meadow soils from the area recently invaded by the Japanese beetle Popillia japonica in Lombardy, Italy, has been surveyed. Oscheius myriophilus was detected at five out of 18 sites resulting positive to entomopathogenic nematodes (EPN), either alone or together with other genera of EPN, indicating a widespread occurrence. The morphological analysis of the strains retrieved showed that they are morphologically in agreement with those of the type population and with other populations recently described. The phylogenetic analysis supported the sub-grouping of all sequences of O. myriophilus from Lombardy with those present in the databases and a close relationship with O. safricana was observed. The capacity to kill the laboratory host Galleria mellonella was similar to that observed in a previous study related to isolates from P. japonica , although O. myriophilus did not cause significant mortality in laboratory trials with the invasive beetles. The isolates of O. myriophilus from Lombardy were characterised in relation to their infectivity to G. mellonella and response to environmental stress, such as heat tolerance and desiccation. Overall, O. myriophilus appears to be an important component of the EPN community of hay meadow soil in Lombardy and might play a role in the containment of the invasive P. japonica. [ABSTRACT FROM AUTHOR]

The endocannabinoid system is composed by a complex and ubiquitous network of endogenous lipid ligands, enzymes for their synthesis and degradation, and receptors, which can also be stimulated by exogenous compounds, such as those derived from the Cannabis sativa. Cannabis and its bioactive compounds, including cannabinoids and non‐cannabinoids, have been extensively studied in different conditions. Recent data have shown that the endocannabinoid system is responsible for maintaining the homeostasis of various skin functions such as proliferation, differentiation and release of inflammatory mediators. Because of their role in regulating these key processes, cannabinoids have been studied for the treatment of skin cancers and melanoma; their anti‐tumour effects regulate skin cancer progression and are mainly related to the inhibition of tumour growth, proliferation, invasion and angiogenesis, through apoptosis and autophagy induction. This review aims at summarising the current field of research on the potential uses of cannabinoids in the melanoma field. [ABSTRACT FROM AUTHOR]

Background: Ubiquilin-4 (UBQLN4), a member of the ubiquilin family, has received limited attention in cancer research to date. Here, we investigated for the first time the functional role and mechanism of UBQLN4 in non-small cell lung cancer (NSCLC). Methods: The Cancer Genome Atlas (TCGA) database was employed to validate UBQLN4 as a differentially expressed gene. Expression differences of UBQLN4 in NSCLC cells and tissues were assessed using immunohistochemistry (IHC) experiment and western blotting (WB) experiment. Kaplan-Meier analysis was conducted to examine the association between UBQLN4 expression and NSCLC prognosis. Functional analyses of UBQLN4 were performed through cell counting kit-8 (CCK-8), colony formation, and transwell invasion assays. The impact of UBQLN4 on tumor-associated signaling pathways was assessed using the path scan intracellular signaling array. In vivo tumorigenesis experiments were conducted to further investigate the influence of UBQLN4 on tumor formation. Results: UBQLN4 exhibited up-regulation in both NSCLC tissues and cells. Additionally, over-expression of UBQLN4 was associated with an unfavorable prognosis in NSCLC patients. Functional loss analyses demonstrated that inhibiting UBQLN4 could suppress the proliferation and invasion of NSCLC cells in both in vitro and in vivo settings. Conversely, functional gain experiments yielded opposite results. Path scan intracellular signaling array results suggested that the role of UBQLN4 is associated with the PI3K/AKT pathway, a correlation substantiated by in vitro and in vivo tumorigenesis experiments. Conclusion: We validated that UBQLN4 promotes proliferation and invasion of NSCLC cells by activating the PI3K/AKT pathway, thereby facilitating the progression of NSCLC. These findings underscore the potential of targeting UBQLN4 as a therapeutic strategy for NSCLC. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of miR-27a on Proliferation, invasion and migration of cutaneous squamous cell carcinoma (CSCC) cells and its targeting relationship with forkhead box G1 (FOXG1). Methods: 30 cases CSCC tissues and 30 cases normal skin tissues were collected. A431 cells were cultured. miR-NC, miR-27a mimics, si-NC, si-miR-27a, Scramble, si-FOXG1, Vector, and OE-FOXG1 plasmids were transfected into the cells and defined as miR-NC group, miR-27a group, si-NC group, si-miR-27a group, Scramble group, si-FOXG1 group, Vector group and FOXG1 group. The si-FOXG1 and Scramble plasmids were transfected into the cells of miR-27a group and recorded as miR-27a+Scramble group and miR-27a+si-FOXG1 group. The cell Proliferation ability was detected by tetramethylazole blue (MTT). The cell invasion and migration ability were detected by Transwell assays. FOXG1 gene mRNA and miR-27a level were detected by fluorescence quantitative polymerase chain reaction (RT-PCR). FOXG1 protein level were detected by Western blot. TargetScan online website was used to predict the binding site of miR-27a and FOXG1. Dual luciferase reporter gene assay was used to verify the targeting relationship between miR-27a and FOXG1. Results: The levels of FOXG1 gene mRNA and miR-27a in CSCC tissues were higher than normal skin tissues (P<0.05), and the levels of FOXG1 gene mRNA in CSCC tissues were positively correlated with and miR-27a level (r=0.801, P=0.000). Up-regulation of miR-27a and FOXG1 promoted cell proliferation, invasion and migration, and silencing of miR-27a and FOXG1 inhibited cell proliferation, invasion, migration and EMT. Down-regulation of miR-27a reversed the the promotive effect of cell Proliferation, invasion and migration by overexpression of FOXG1. miR-27a positively regulated FOXG1 expression. Conclusion: miR-27a and FOXG1 are highly expressed in CSCC tissues. miR-27a positively regulates FOXG1 to promote proliferation, invasion, and migration of CSCC cells. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of calcium and integrin-binding protein 1 (CIB1) on the cell proliferation, invasion, apoptosis, and migration of triple-negative breast cancer cells and its possible mechanism. Methods MDA-MB-231 and MDA-MB-468 cells were divided into CIB1-knockdown (infected with CRISPR/Cas9 lentivirus) and negative-control groups. Cell Counting Kit-8 (CCK-8) and 5- ethynyl-2 ′-deoxyuridine (EdU) assays were performed to detect cell proliferation. Cell apoptosis was determined through flow cytometry. Scratch and Transwell experiments were conducted to measure the migration and invasion abilities of cells. The mRNA and protein expression levels of β-catenin, adenomatous polyposis coli (APC), glycogen synthase kinase 3β (GSK-3β), and c-myc were detected via real-time quantitative polymerase chain reaction and Western blot. Results Compared with the negative-control group, the CIB1-knockdown group showed decreased cell proliferation, invasion, and migration (P<0.05) and increased cell apoptosis (P<0.05). The mRNA and protein expressions of β-catenin, APC, and c-myc decreased (P<0.05), and that of GSK-3β increased (P<0.05). Conclusion CIB1 knockdown can inhibit cell proliferation, invasion, and migration and promote the apoptosis of breast cancer cells. Its mechanism may be related to the inhibition of Wnt/β-catenin signaling pathway [ABSTRACT FROM AUTHOR]

Placenta accreta spectrum (PAS) refers to excessive placental invasion into the maternal uterus and it is associated with high risk of obstetric haemorrhage and adverse maternal-neonatal outcomes. Currently, no specific circulating biomarkers of PAS have been identified. Given that in PAS disorders, the depth and the extension of placental invasion into the uterus are expected to be increased, in this study, we analysed plasma levels of syncytiotrophoblast-derived extracellular vesicles (STBEVs) in women with placenta previa (PP), at a high risk of PAS disorders, and pregnant women with normal placentation. Venous blood samples were collected from 35 women with ultrasonographic diagnosis of PP and 35 women with normal placentation, matched for gestational age. Plasma samples were ultracentrifuged at 120.000 g to collect extracellular vesicles (EVs). To identify and quantify plasma placenta–derived EVs (or STBEVs), EVs were analysed by flow cytometry using a monoclonal antibody against placental alkaline phosphatase (PLAP). Plasma levels of STBEVs were significantly higher in PP patients compared to controls. Plasma levels of STBEVs in women with PP and PAS showed a trend to a higher concentration compared to women with PP without PAS, although not reaching a statistical significance. Circulating STBEVs are potential candidates as biological markers to be integrated to ultrasonography in the antenatal screening programme for PAS. More studies are needed to confirm our observation in a larger cohort of patients and to analyse a possible association between high circulating levels of STBEVs and PAS. [ABSTRACT FROM AUTHOR]

The idea of a Jewish invasion in Romania appeared during the debates on the first constitution (1866) and was revitalized after 1918, as the recently occupied territory of Bessarabia hosted many Jewish groups fleeing revolutionary Russia, the civil war, and pogroms. In this context, the immigrants were depicted by nationalist propaganda as invaders wishing to exploit Romania's wealth and hospitality, and this image was combined with the myth of Judeo-Bolshevism. Thanks to the archival sources of the High Commission for Refugees and of relief organizations such as the Joint Distribution Committee, this paper aims to present in detail the controversial encounter between national security policies and humanitarian concerns for the fate of the refugees. At the same time, it will discuss how the refugee question influenced the Romanian political context, fostering sentiments of antisemitism and xenophobic anxiety. As will be argued, the idea of an invasion was very influential before and after World War I, and conditioned not only the definition of the policies regarding citizenship and minorities, but also the whole political discourse and the shaping of Romanian identity. At the same time, the emergence of refugees and the juxtaposition of humanitarian versus national security was not a purely Romanian affair, and in many aspects anticipated the topics of today's debates. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of Lathyrol on the expression of androgen receptor (AR) and sphingosine kinase 2 (SPHK2) in renal cell carcinoma (RCC) mice and to further explore the mechanism by which Lathyrol inhibits the invasion and incidence of epithelial-mesenchymal transition (EMT). Methods: An RCC xenograft mouse model was constructed, and the mice were randomly divided into a model group, an experiment group and a negative control group. The experiment group was intragastrically gavaged with Lathyrol solution (20 mg/kg), the model group was intragastrically gavaged with 0.9% NaCl (same volume as that used in the experiment group), and the negative control group was injected intraperitoneally with 2 mg/kg cisplatin aqueous solution. Changes in the body weight and tumor volume of the mice were recorded. Western blot (WB) was used to assess the protein expression levels of AR, p-AR, CYP17A1, PARP1, E-cadherin, N-cadherin, vimentin, α-SMA, β-catenin, and ZO-1. Protein expression levels of SPHK2, metal matrix protease 2 (MMP2), MMP9 and urokinase-type plasminogen activator (uPA) in tumor tissues were assessed by immunohistochemistry (IHC). AR expression in tumor tissues was assessed after immunofluorescence (IF) staining. Results: After 14 days of drug administration, compared with that in the model group, the tumor volumes in the negative control and experiment groups were lower; the difference in tumor volume among the model, control and experiment groups was statistically significant (P < 0.05). The differences in body weight among the three groups were not statistically significant (P > 0.05). In the model group, the protein expression levels of AR, p-AR, CYP17A1, SPHK2, and PARP1 were relatively increased, the protein expression levels of E-cadherin and ZO-1 were relatively reduced (P < 0.05), and the protein expression levels of N-cadherin, β-catenin, vimentin, and α-SMA were relatively increased (P < 0.05). In the negative control and experiment groups, the protein expression levels of AR, p-AR, CYP17A1, SPHK2, and PARP1 were relatively decreased (P < 0.05), the protein expression levels of E-cadherin and ZO-1 were relatively increased (P < 0.05), and the protein expression levels of N-cadherin, β-catenin, vimentin and α-SMA were relatively decreased (P < 0.05). Conclusion: Lathyrol and cisplatin inhibit the proliferation of RCC xenografts, reduce the protein expression levels of AR, CYP17A1, SPHK2, PARP1, E-cadherin, and ZO-1 in tumor tissues (P < 0.05), and promote the protein expression levels of N-cadherin, β-catenin, vimentin and α-SMA (P < 0.05). Therefore, Lathyrol reduces RCC invasion and EMT by affecting the expression of AR and SPHK2 in RCC mice. [ABSTRACT FROM AUTHOR]

Background: Lysyl oxidase enzymes (LOXs), as extracellular matrix (ECM) protein regulators, play vital roles in tumor progression by remodeling the tumor microenvironment. However, their roles in glioblastoma (GBM) have not been fully elucidated. Methods: The genetic alterations and prognostic value of LOXs were investigated via cBioPortal. The correlations between LOXs and biological functions/molecular tumor subtypes were explored in The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA). After Kaplan‒Meier and Cox survival analyses, a Loxl1-based nomogram and prognostic risk score model (PRSM) were constructed and evaluated by time-dependent receiver operating characteristic curves, calibration curves, and decision curve analyses. Tumor enrichment pathways and immune infiltrates were explored by single-cell RNA sequencing and TIMER. Loxl1-related changes in tumor viability/proliferation and invasion were further validated by CCK-8, western blot, wound healing, and Transwell invasion assays. Results: GBM patients with altered LOXs had poor survival. Upregulated LOXs were found in IDH1-wildtype and mesenchymal (not Loxl1) GBM subtypes, promoting ECM receptor interactions in GBM. The Loxl1-based nomogram and the PRSM showed high accuracy, reliability, and net clinical benefits. Loxl1 expression was related to tumor invasion and immune infiltration (B cells, neutrophils, and dendritic cells). Loxl1 knockdown suppressed GBM cell proliferation and invasion by inhibiting the EMT pathway (through the downregulation of N-cadherin/Vimentin/Snai1 and the upregulation of E-cadherin). Conclusion: The Loxl1-based nomogram and PRSM were stable and individualized for assessing GBM patient prognosis, and the invasive role of Loxl1 could provide a promising therapeutic strategy. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer is the third most common malignancy worldwide and is one of the leading causes of cancer‐related mortality. Ubiquitin‐specific peptidase 18 (USP18) protein has been reported to exert different tumor‐related effects in distinct tumor types. Here, we initially investigated the expression and signaling pathways of USP18 in colon adenocarcinoma (COAD). Methods: A quantitative real‐time PCR was conducted to evaluate the mRNA level of USP18 in cultured cells. Immunohistochemical staining was used to explore the protein expression of USP18 in clinical COAD samples. Specific knockdown was achieved by transient transfection of small interfering RNAs into SW480 and HT29 cells using Lipo3000. Cell conting kit‐8 assay, transwell assay and matrigel‐transwell assays were conducted to evaluate proliferation, migration and invasion capacities, respectively. Western blotting was performed to analyze downstream signaling pathways. A chi‐squared test and univariate and multivariate analyses were used to evaluate the clinical data. Xenografts from mice model were assessed to validate the in vitro findings. Results: Higher USP18 level was identified in COAD tissues and was positively correlated with advanced tumor stage. High USP18 protein expression indicated poorer prognosis of COAD patients. Silencing USP18 suppressed COAD cell proliferation and invasion via destabilizing extracellular signal‐regulated kinase (ERK) protein and suppressing ERK downstream pathways. Simultaneously silencing interferon‐stimulated gene 15 (ISG15) with USP18 can partially rescue the tumor cell viability, indicating its involvement in USP18 signaling. The oncogenic effects of USP18 were also confirmed in mice models. Conclusions: USP18 plays oncogenic effects in colon adenocarcinoma via ISG15‐ERK pathways. High USP18 expression indicates poor clinical outcomes for colon adenocarcinoma patients. [ABSTRACT FROM AUTHOR]

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