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Range expansions, whether they are biological invasions or climate change-mediated range shifts, may have profound ecological and evolutionary consequences for plant-soil interactions. Range-expanding plants encounter soil biota with which they have a limited coevolutionary history, especially when introduced to a new continent. Past studies have found mixed results on whether plants experience positive or negative soil feedback interactions in their novel range, and these effects often change over time. One important theoretical explanation is that plants locally adapt to the soil pathogens and mutualists in their novel range. We tested this hypothesis in Dittrichia graveolens, an annual plant that is both expanding its European native range, initially coinciding with climate warming, and rapidly invading in California after human introduction. In parallel greenhouse experiments on both continents, we used plant genotypes and soils from five locations at the core and edge of each range to compare plant growth in soil inhabited by D. graveolens and nearby control microsites as a measure of plant-soil feedback. Plant-soil interactions were highly idiosyncratic across each range. On average, plant-soil feedbacks were more positive in the native range than in the exotic range. In line with the strongly heterogeneous pattern of soil responses along our biogeographic gradients, we found no evidence for evolutionary differentiation between plant genotypes from the core to edge of either range. Our results suggest that the evolution of plant-soil interactions during range expansion may be more strongly driven by local evolutionary dynamics varying across the range than by large-scale biogeographic shifts.

Changes in substrate quality driven by climate, land use, or other forms of global change may represent a strong selective force on microbial communities. Invasion of new taxa into a community through dispersal, evolution, or recolonization could impact the outcome of this environmental selection. Here, we simulated substrate change with a trait-based model of microbial litter decomposition (DEMENTpy) to assess the legacy effects of past substrate quality and the impact of selection by a new substrate on community decomposition activity. Simulations were run with different levels of invasion, including invasion from communities long-adapted to the new substrate. Legacy effects were evident with substrate change for native communities differing in composition. Protein was the only substrate that exerted a strong enough selective force to affect community composition. Legacy effects disappeared when invaders came from substrates similar to the new substrate. Together, our simulations demonstrate that substrate quality changes associated with global change can lead to legacy effects on substrate degradation. In decomposing plant litter, such legacy effects can occur if substrate inputs shift to higher protein content and if invasion is low.

Recent studies confirm the critical roles of endoplasmic reticulum oxidoreductase 1 alpha (ERO1L) in malignant behavior of various cancers. Nevertheless, what function ERO1L plays in lung adenocarcinoma (LUAD) remains uncovered. The expressions and clinical significance of ERO1L in LUAD were investigated using the TCGA dataset. The ERO1L levels were examined by RT-qPCR. The LUAD cell proliferation was valued using colony formation as well as CCK-8 assays. The invasion and migration abilities of LUAD cells were detected through Transwell in addition to wound healing assays. The effects of ERO1L on LUAD cell apoptosis were determined by flow cytometric analysis. Moreover, we also established mouse xenograft models of LUAD cells to confirm the functions of ERO1L in vivo. The ERO1L levels in tumors were identified by immunohistochemistry. Western blot was used for the detection of the levels of Wnt/βcatenin signaling-related proteins. The TCGA database revealed that ERO1L expressions were higher in LUAD tissues than those in non-cancerous tissues. ERO1L overexpression was related to poorer overall survival of LUAD patients. In addition, ERO1L silence suppresses LUAD cell clone formation, proliferation, migration as well as invasion but induces apoptosis. Moreover, we also verified that ERO1L silence could promote LUAD growth in vivo. Based on the mechanism analysis, ERO1L was confirmed to regulate LUAD development via Wnt/βcatenin cascade signal. ERO1L, the expression of which was increased in LUAD tissues, functioned as an oncogene. ERO1L silence significantly attenuated LUAD tumorigenesis, likely via inhibition of Wnt/βcatenin signaling, indicating that ERO1L could be exploited as a promising biomarker in LUAD treatment. [ABSTRACT FROM AUTHOR]

Gossypol, a natural polyphenolic compound, possesses antivirus activity and induces cell death of different types of tumors. However, the efficacy of gossypol on lung carcinoma metastases and epithelial to mesenchymal transition remains unknown. The aim of the present work was to determine the cellular and molecular mechanism of the anti‐cancer and anti‐metastatic efficacies of gossypol on human lung carcinoma cells. Gossypol showed a marked suppression of the viability, motility, and invasion in H1299 and A549 cells. Zymography assay showed that gossypol was sufficient to suppress the activities of urokinase‐type plasminogen activator and matrix metalloproteinase‐2. Gossypol reversed TGF‐β‐induced epithelial to mesenchymal transition. Gossypol reduced vimentin, p‐FAK, p‐Src and p‐paxillin. In vivo studies of gossypol were performed using subcutaneous inoculation and tail vein injection of A549 into immunodeficient BALB/c nude mice and severe combined immunodeficient mice. [ABSTRACT FROM AUTHOR]

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In this paper, we examine a predator–prey model with general reaction functions in open advective environments, where the predator and prey may employ distinct movement strategies. Using the coefficients of diffusion and advection as varying parameters, we conduct a quantitative analysis on the critical advection rates, which distinguish the different dynamics of this predator–prey system, to explore the joint impact of advection and diffusion on the invasion and coexistence of predators and prey in an open flow. It turns out that the dynamics may switch many times between a successful or failed invasion, coexistence or generalist predator take-over as the advection and diffusion rates of predators and prey vary, which suggests that both diffusion and advection play a crucial role in shaping the dynamics of the predator–prey system. [ABSTRACT FROM AUTHOR]

Although the impacts of single-species invasions on resident communities have been widely studied, the ecological effects of co-invasion (simultaneous invasion by multiple alien species) remain largely unexplored. In this study, using an analytical framework, we investigate the individual and combined effects of two global plant invaders (Leucanthemum vulgare and Lupinus polyphyllus) on the aboveground vegetation (plant richness, diversity and biomass) and belowground soil variables (pH, salinity, electrical conductivity, total dissolved solids, organic carbon [OC], phosphorous, and potassium) of grassland communities in the Himalaya. We studied these ecological variables in comparable plots under the following four scenarios: both invaders absent (i.e. uninvaded), either of the two invaders present (i.e. single species invasion), and both invaders present (i.e., co-invasion). Our results show invasion effects vary with the invasion scenarios and the studied variables. The single species invasion plots had lower mean plant richness and diversity but higher mean soil OC than the uninvaded plots. The co-invasion plots had significantly increased mean plant biomass and soil OC, but had a non-significant effect on plant richness and diversity compared to the uninvaded plots. The overall combined effect of species' co-invasion was additive in nature, but the effect varied significantly with choice of the response variable. We found synergistic effects of co-invasion on species richness and diversity, antagonistic effects on soil pH, and additive effects on the remaining response variables when compared with the predicted additive effect of the two invaders. Our findings suggest that further spread of L. polyphyllus will impact the resident plant community more severely when co-invading with L. vulgare than when invading alone, thereby lending support to the invasional meltdown hypothesis. Nevertheless, antagonistic and additive impacts for soil pH and other response variables respectively hint towards other alternate mechanisms at play. Overall, our study showcases a proof-of-concept to empirically estimate the additive, antagonistic and synergistic impacts of plant co-invasions, and also provides a model for designing co-invasion studies on other taxa/systems/scales elsewhere. Finally, based on the insights gained from this study, we highlight priority areas of future research in species' co-invasions. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) has a fatal prognosis because of its aggressive and invasive characteristics. Understanding the mechanism of invasion necessitates an elucidation of the relationship between tumor cells and the tumor microenvironment. However, there has been a scarcity of suitable models to investigate this. In this study, we established a glioblastoma‐cerebral organoid assembloid (GCOA) model by co‐culturing patient‐derived GBM tumoroids and human cerebral organoids. Tumor cells from the tumoroids infiltrated the cerebral organoids, mimicking the invasive nature of the parental tumors. Using time‐lapse imaging, various invasion patterns of cancer cells within cerebral organoids resembling a normal tissue milieu were monitored. Both single‐ and collective‐cell invasion was captured in real‐time. We also confirmed the formation of an intercellular tumor network and tumor–normal‐cell interactions. Furthermore, the transcriptomic characterization of GCOAs revealed distinct features of invasive tumor cells. Overall, this study established the GCOA as a three‐dimensional (3D) in vitro assembloid model to investigate invasion mechanisms and interactions between tumor cells and their microenvironment. [ABSTRACT FROM AUTHOR]

The relative rates of sexual versus asexual reproduction influence the partitioning of genetic diversity within and among populations. During range expansions, asexual reproduction often facilitates colonization and establishment. The arrival of the green alga Avrainvillea lacerata has caused shifts in habitat structure and community assemblages since its discovery in 1981 offshore of Oʻahu, Hawai‘i. Field observations suggest this species is spreading via vegetative reproduction. To characterize the reproductive system of A. lacerata in Hawai‘i, we developed seven microsatellite loci and genotyped 321 blades collected between 2018 and 2023 from three intertidal sites at Maunalua Bay and ʻEwa Beach. We observed one to four alleles at multiple loci, suggesting A. lacerata is tetraploid. Each site was characterized by high genotypic richness (R > 0.8). However, clonal rates were also high, suggesting the vegetative spread of A. lacerata plays a significant role. The importance of clonal reproduction for the persistence of A. lacerata in Hawai‘i is consistent with the ecological data collected for this species and observations of other abundant macroalgal invaders in Hawai‘i and other regions of the world. These data demonstrate the necessity for implementing appropriate population genetic methods and provide insights into the biology of this alga that will contribute to future studies on effective management strategies incorporating its reproductive system. This study represents one of the few that investigate green algal population genetic patterns and contributes to our understanding of algal reproductive system evolution. [ABSTRACT FROM AUTHOR]

Birds are among the organisms most impacted by plant invasions, the effects of which are particularly conspicuous during the breeding season. Birds can incorrectly assess the suitability of large, invasive hogweeds Heracleum sp. in south‐eastern Poland when selecting nesting sites early in spring when the developing invaders do not yet differ substantially in form from the rest of the vegetation. One would expect lower bird breeding success in areas with invasive hogweeds. Furthermore, this may shift bird community composition towards species with filtered traits, which may then be reflected in various measures of diversity. To assess these expectations, we conducted bird surveys at 74 sites, arranged as 37 pairs (with invasive Heracleum vs. control). The presence of Heracleum was associated with lower bird taxonomic and phylogenetic diversity. Functional richness (calculated based on species' reproductive traits) was also lower at sites with these invaders. The species detected at Heracleum sites were characterised by traits associated with rapid breeding, for example, small clutches, short incubation periods and short fledging periods. We show that the bird community at sites with hogweeds became less diverse and composed of random species sharing similar reproductive traits. Bird communities with low diversity at Heracleum sites tended to exhibit a common trait syndrome. These patterns provide insights into the mechanisms of how invasive plants may lead to the loss of some traits and species in bird communities. Read the free Plain Language Summary for this article on the Journal blog. [ABSTRACT FROM AUTHOR]

ABSTRACT The threespine stickleback, Gasterosteus aculeatus, has undergone dramatic increases in abundance in parts of its historical native range, and it is also undergoing a major range expansion. We review available information and discuss the vectors and sources of the species' range expansions, the genetic characteristics of recently founded populations and the ecological consequences of both stickleback introductions and increases in abundance. Dramatic range expansions occurred in the Caspian Sea drainage, large rivers in the Black Sea drainage, reservoirs of the Rhine basin, isolated lakes in North America and Japan and remote islands in the Arctic. Likely reasons for these range expansions include canal construction, accidental inclusion with stocking of commercially valuable fish, intentional release by aquarists and fishermen and climate change. In some cases, range expansions of stickleback were likely facilitated by genetic admixture of previously separated lineages, as well as by high‐standing genetic variation that promotes rapid adaptation to new habitats. Accordingly, range expansions are often accompanied by striking increases in abundance, although these are two distinct processes. Notably, population growth within the species' native range, particularly in the White and Baltic Seas, has been observed alongside expansions into new areas. Where stickleback colonise new habitats or increase in abundance, extensive ecological impacts on ecosystems typically occur. Given these massive and widespread changes, the species has the potential to provide considerable insight into the evolutionary and ecological effects of human impacts on aquatic ecosystems. [ABSTRACT FROM AUTHOR]

Background: Intradural lipomas have been previously reported in individuals with spinal dysraphism; however, they have not been reported in cats with an intact spinal canal. Desmoid tumors are a rare finding in veterinary medicine, and there is no prior description of these tumors invading the spinal cord. Furthermore, the etiopathogenesis remains debated, with trauma, such as surgical intervention of an intradural structure, potentially contributing to its development. Case description: A 10-month-old domestic shorthair cat was presented initially with progressive proprioceptive ataxia. The MRI identified an intradural compressive lesion at the cranio-cervical junction, confirmed as a lipoma by histopathology. Despite surgical removal, postoperative complications led to the cat's euthanasia. Postmortem examination revealed invasion of a desmoid tumor at the surgical site. Conclusions: This case highlights the rarity of intradural lipomas in this location and the unusual complication of desmoid tumor invasion. It underscores the need for further research into the underlying mechanisms and potential diagnostic and therapeutic strategies for similar cases and suggests that these findings may be added to the list of potential post-surgical complications. [ABSTRACT FROM AUTHOR]

The discovery of embryonic stem cell (ESC) mediating tumoricidal activity revealed the intimate relationship between ESCs and tumor cells, but the functional role of ESCs in tumor progression is poorly understood. To further investigate tumor cell and ESC interactions, we co-cultured mouse ESCs with mouse pancreatic cancer Pan02 cells or mouse melanoma B16-F10 cells in Transwell, and found that tumor cell invasion was significantly inhibited by ESCs. Application of ESCs to tumor-bearing mice resulted in significant inhibition of tumor metastasis in vivo. RNA-Seq analyses of tumor cell and ESC co-cultures identified TP53 and related signalling as major pathways involved in ESC-mediated inhibition of tumor cell invasion and metastasis, which indicated the potential clinical application of ESCs to treat cancer. [ABSTRACT FROM AUTHOR]

Escherichia coli K1 is the leading cause of neonatal gram-negative bacterial meningitis, but the pathogenesis of E coli K1 meningitis remains unclear. Blood-brain barrier (BBB) penetration is a crucial step in E coli meningitis development. Here, we uncovered the crucial role of CsiR, a GntR family regulator, in E coli K1 virulence. During infection, csiR expression was induced due to the derepression by Fur in the blood and human brain microvascular endothelial cells (HBMECs). CsiR positively regulated ilvB expression, which is associated with branched chain amino acid synthesis. Furthermore, we revealed that IlvB activated the FAK/PI3K pathway of HBMECs to induce actin cytoskeleton rearrangements, thereby promoting the bacterial invasion and penetration of the BBB. Overall, this study reveals a CsiR-mediated virulence regulation pathway in E coli K1, which may provide a useful target for the prevention or therapy of E coli meningitis. [ABSTRACT FROM AUTHOR]

Background: Intramuscular hemangioma is a vascular malformation occurring in muscle tissues. It is most common in skeletal muscles of limbs, especially lower limbs in childhood. The intercostal intramuscular hemangioma with sternal invasion is very rare. Case presentation: The 47-year-old female patient was hospitalized due to "suddenly chest pain for 4 days". Chest contrast-enhanced CT indicated bony changes in the sternum, accompanied by soft tissue shadows in the posterior sternum and diaphragmatic angle. After admission, physical examination showed: peristernal tenderness, percussion pain, other no obvious positive signs. PET-CT examination indicated that there was a high possibility of benign sternal changes. No cancer cells were found by sternal puncture. Surgical biopsy was performed and pathological findings were consistent with intramuscular hemangioma. Conclusion: Intramuscular hemangioma with bone invasion is very rare, imaging examination is difficult to indicate obvious evidence, preoperative diagnosis is difficult, complete surgical resection is very important, more personalized treatment should be provided according to the overall situation of the patient. [ABSTRACT FROM AUTHOR]

Uterine corpus endometrial carcinoma (UCEC) is one of the most common tumours of the female reproductive system. CCAAT enhancer-binding protein alpha (CEBPA) is a member of the transcription factor family involved in regulating processes such as cell proliferation, differentiation, metabolism, and the immune response. However, the role of CEBPA in UCEC has not been clarified. Here, we performed a comprehensive analysis to explore the expression level, prognostic value, immune infiltration and biological function of CEBPA in UCEC. In this study, we found that CEBPA expression was upregulated and associated with poor prognosis in UCEC patients. KEGG and GO analyses revealed that the genes positively correlated with CEBPA were enriched primarily in immune regulation and oxidative phosphorylation. Immune infiltration analysis revealed that CEBPA is strongly correlated with immune cell infiltration in UCEC. RT-qPCR indicated that CEBPA may regulate the OXPHOS level in Ishikawa cells. CCK-8, cell cycle, Transwell and scratch wound healing assays revealed that CEBPA promoted Ishikawa cell proliferation, invasion and migration. In addition, PPI and survival analyses suggested that CEBPG may be a potential target of CEBPA in UCEC. These results demonstrated that CEBPA may be a potential therapeutic target in UCEC. [ABSTRACT FROM AUTHOR]

Background: Existing studies have already revealed the involvement of C–C chemokine receptor type 7 (CCR7) in diverse human cancers, including esophageal cell squamous carcinoma (ESCA). Our current study, aims to explore the relevant mechanisms implicated. Methods: ESCA cell lines were collected for CCR7 expression quantification using western blot. Following the transfection, the viability, migration and invasion of ESCA cells were evaluated via cell counting kit-8 and Transwell assays. The specific molecular mechanisms underlying the effects of CCR7 in ESCA cells were explored via calculating the expressions of proteins related to metastasis and Janus kinase 2/signal transduction and transcription activation 3 (JAK2/STAT3) signaling pathway via western blot. The correlation between CCR7 and metastasis-related proteins was explored via Pearson's correlation test. Results: CCR7 was high-expressed in ESCA cells and CCR7 knockdown repressed the viability, migration and invasion of ESCA cells, concurrent with the increased expression of E-cadherin (E-cad, which was also known as CDH1 and lowly expressed in ESCA cells) and the decreased expressions of vimentin (Vim, which was highly expressed in ESCA cells) and matrix metalloproteinase-9 (MMP-9, which was also highly expressed in ESCA cells). Meanwhile, CCR7 was positively correlated with Vim and MMP-9 yet negatively correlated with E-cad in ESCA cells, which indicated that CCR7 has a role in promoting tumor progression in ESCA cells. Besides, the phosphorylation of STAT3 and JAK2 in ESCA cells was elevated, which was diminished following CCR7 knockdown. Conclusion: This study proves the modulation of CCR7 on ESCA in vitro, which was achieved via JAK2/STAT3 signaling pathway. Our discovery will provide new therapeutic basis and insights for ESCA. [ABSTRACT FROM AUTHOR]

Annual ryegrass (Lolium rigidum) is a problematic weed in winter crops and fallows in the southeastern cropping region (SCR) of Australia. This weed has evolved resistance to multiple herbicide groups, globally. In Australia, L. rigidum is more prevalent in the western and southern regions than in SCR. To assess the herbicide resistance status of L. rigidum, the response of five L. rigidum populations (collected from the SCR) to glyphosate, glufosinate, paraquat, haloxyfop-P-ethyl, and clethodim is determined using dose–response curves. Three parametric logistic models are used to determine the herbicide dose required to achieve 50% survival (LD50) and 50% growth reduction (GR50). The LD50 values for 50% survival at 28 days after treatment range from 1702 g a.e. ha−1 to 8225 g a.e. ha−1 for glyphosate, 1637 g a.i. ha−1 to 1828 g a.i. ha−1 for glufosinate, 141 g a.i. ha−1 to 307 g a.i. ha−1 for paraquat, 11 g a.i. ha−1 to 107 g a.i. ha−1 for haloxyfop-P-ethyl, and 17 g a.i. ha−1 to 48 g a.i. ha−1 for clethodim. The resistance factor, based on GR50 value, is highest in the S7 population (2.2 times) for glyphosate, the S11 population (2.3 times) for glufosinate, the S11 population (2.0 time) for paraquat, the S7 population (3.9 times) for haloxyfop-P-ethyl, and the S3 population (3.1 times) for clethodim, compared with the susceptible or less tolerant population. The S11 population is found to be resistant to five tested herbicides, based on resistance factors. Similarly, the S3 population is highly resistant to glyphosate, haloxyfop-P-ethyl, and clethodim compared with the W4 population. These results suggest that L. rigidum populations in the SCR exhibit resistance to multiple herbicide groups at labelled field rates. The findings highlight the necessity of adopting an integrated management approach, including the use of residual herbicides, tank mixing herbicides with different modes of action, and rotating herbicides in conjunction with cultural and mechanical control methods. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of long non-coding RNA LINC00261 in regulating E26 transcription factor 1 (EST1) by interfering with the expression of miR-324-3p in promoting the development of gastric cancer (GC). Methods: Cancer tissues and corresponding adjacent normal tissues of GC patients (n=80) who underwent surgical treatment in 363 Hospital from June 2018 to October 2020 were collected as research samples, and the expression levels of LINC00261 and miR-324-3p were detected by qRT-PCR. The correlation between LINC00261 and clinicopathological parameters were analyzed. siRNA (si-LINC00261), miRNA mimic (miR-324-3p), miRNA inhibitor (miR-324-3p in) and their corresponding controls were transfected into MGC-803 and SGC- 7901 cells. Clonogenesis assay was used to evaluate cell proliferation. The Transwell assay assessed cell migration and invasion. The protein expression levels of E-cadherin, N-cadherin and ETS1 were detected by Western blot. Tumor xenotransplantation assay was used to detect the tumorigenesis of LINC00261 in vivo. Luciferase report and RNA precipitation were used to analyze the interaction between LINC00261, miR-324-3p and EST1. Results: Compared with adjacent tissues, the expression of LINC00261 in GC tissues was significantly up-regulated with statistical significance (P<0.05). The expression of LINC00261 was correlated with TNM stage, tissue differentiation degree, lymph node metastasis and microvascular invasion (P<0.05). The database prediction, firefly luciferase assay and RNA immunoprecipitation results showed that LINC00261 had a targeted relationship with miR-324-3p. The level of miRdoi: 324-3p in GC tissues was significantly lower than that in paracellular normal tissues (P<0.05). There was a negative correlation between miR-324-3p level and LINC00261 expression (P<0.05). Compared with in NC+si-NC group, the cell proliferation, migration and invasion ability and the expression of N-cadherin in in NC+si-LINC00261 group were significantly inhibited (P<0.05), while the expression of E-cadherin was significantly increased (P<0.05). Compared with in NC+si-LINC00261 group, cell proliferation, migration and invasion ability and expression of N-cadherin in si-LINC00261+miR-324-3p in group were significantly increased (P<0.05), while the expression of E-cadherin was significantly decreased (P<0.05). Targetscan prediction and firefly luciferase assay showed that ETS1 was the downstream binding site of miR-324-3p. After transfection with miR-324-3p, ETS1 protein level was significantly down-regulated (P<0.05), but after transfection with miR-324-3p in, ETS1 protein level was significantly up-regulated (P<0.05). The expression of ETS1 in GC tissue was significantly higher than that in adjacent normal tissue (P<0.05). The miR-324-3p level was negatively correlated with ETS1 (P<0.05). The tumor weight of MGC-803 cells transfected with si-LINC00261 was lower than that of MGC-803 cells transfected with si-NC (P<0.05), and the protein level of ETS1 in si-LINC00261-derived tumors was lower than that of si-NC tumors (P<0.05). Conclusion: LINC00261 is highly expressed in GC tissue, which may affect EST1 expression and promote GC progress by regulating miR-324-3p. [ABSTRACT FROM AUTHOR]

Background: Invasion is an important characteristic of the malignancy of glioblastoma (GBM) and a significant prognostic factor. Sempervirine (SPV), a yohimbine-type alkaloid, has been proven to inhibit GBM cells proliferation in previous research and found to have a potential effect in anti-invasion, but its mechanism of anti-invasion is still unknown. Methods: To explore its pharmacodynamics in inhibiting GBM cell invasion in this study, we combined network pharmacology and bioinformatics to comprehensive exploratory analysis of SPV and verified the mechanism in vitro. Results: Firstly, targets of SPV and invasion-related genes were collected from public databases. Moreover, GBM samples were obtained to analyze differentially expressed genes (DEGs) from The Cancer Genome Atlas (TCGA). Then, the relevant targets of SPV inhibiting GBM invasion (SIGI) were obtained through the intersection of the three gene sets. Further, GO and KEGG analysis showed that the targets of SIGI were heavily enriched in the AKT signaling pathway. Subsequently, based on the method of machine learning, a clinical prognostic model of the relevant targets of SIGI was constructed using GBM samples from TCGA and the Gene Expression Omnibus (GEO). A four-genes model (DUSP6, BMP2, MMP2, and MMP13) was successfully constructed, and Vina Scores of MMP2 and MMP13 in molecular docking were higher, which may be the main targets of SIGI. Then, the effect of SIGI was confirmed via functional experiments on invasion, migration, and adhesion assay, and the effect involved changes in the expressions of p-AKT, MMP2 and MMP13. Finally, combined with AKT activator (SC79) and inhibitor (MK2206), we further confirmed that SPV inhibits GBM invasion through AKT phosphorylation. Conclusions: This study provides valuable and an expected point of view into the regulation of AKT phosphorylation and inhibition of GBM invasion by SPV. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by synovial hyperplasia, and fibroblast‐like synoviocytes (FLSs) constitute the majority of cells in the synovial tissue, playing a crucial role in the onset of RA. Dysregulation of FLSs function is a critical strategy in treating joint damage associated with RA. Non‐coding RNAs, a class of RNA molecules that do not encode proteins, participate in the development of various diseases. This article aims to review the progress in the study of long non‐coding RNAs, microRNAs, and circular RNAs in FLSs. Non‐coding RNAs are involved in the pathogenesis of RA, directly or indirectly regulating FLSs' proliferation, migration, invasion, apoptosis, and inflammatory responses. Furthermore, non‐coding RNAs also influence DNA methylation and osteogenic differentiation in FLSs. Therefore, non‐coding RNAs hold promise as biomarkers for diagnosing RA. Targeting non‐coding RNAs in FLSs locally represents a potential strategy for future therapies in RA. [ABSTRACT FROM AUTHOR]

Background: Actin-like protein 8 (ACTL8) significantly correlates with tumor growth and prognosis across various cancer types. Nevertheless, the potential relationship between ACTL8 and gastric cancer (GC) remains uncertain. Objective: This study aimed to elucidate the role of ACTL8 in human GC cells and to explore its mechanism. Methods: Bioinformatics analysis tools, such as GEPIA2, Kaplan–Meier, and STRING, were utilized for a comprehensive investigation of the characteristics and functional roles of ACTL8 in GC, including differential expression, prognostic value, and related signaling pathways. Subsequently, gene expression analyses, cell function assays, and signaling pathway experiments were conducted to verify key findings. Results: Bioinformatics analysis showed that ACTL8 was significantly elevated in GC and closely associated with poor prognosis. Gene expression experiments confirmed the bioinformatics results. Furthermore, ACTL8 knockdown markedly reduced GC cell proliferation and inhibited migration and invasion. Mechanistically, a significant increase in the phosphorylation levels of signaling proteins was observed in GC cells following ACTL8 overexpression, and PI3K/Akt/mTOR pathway inhibitors could reverse this effect. Conclusion: ACTL8 expression is significantly upregulated in GC cells and is closely correlated with poor patient prognosis. Further mechanistic studies revealed that ACTL8 may promote GC cell migration and proliferation through activation of the PI3K/Akt/mTOR signaling pathway. Consequently, ACTL8 emerges as a promising therapeutic target for GC. [ABSTRACT FROM AUTHOR]

Simple Summary: The role of the GPER in cancer is controversial due to its dual anti and protumor effects. Elevated GPER expression in cervical cancer has been associated with improved survival outcomes. In cervical cancer cell lines, the selective GPER agonist G-1 induces cell cycle arrest and apoptosis, although the precise molecular mechanisms behind these effects are not fully understood. This study explores the impact of GPER activation by G-1 on the transcriptome, cell migration, and invasion in SiHa cells, as well as in non-tumorigenic keratinocytes transduced with HPV16 E6 or E7 oncogenes. G-1 has been shown to exert antitumor effects by activating apoptotic pathways and modulating migration and invasion processes. The findings support the GPER as a promising prognostic marker and suggest that G-1 could be a valuable therapeutic tool for treating cervical cancer. Background/Objectives: Estrogens and HPV are necessary for cervical cancer (CC) development. The levels of the G protein-coupled estrogen receptor (GPER) increase as CC progresses, and HPV oncoproteins promote GPER expression. The role of this receptor is controversial due to its anti- and pro-tumor effects. This study aimed to determine the effect of GPER activation, using its agonist G-1, on the transcriptome, cell migration, and invasion in SiHa cells and non-tumorigenic keratinocytes transduced with the HPV16 E6 or E7 oncogenes. Methods: Transcriptome analysis was performed to identify G-1-enriched pathways in SiHa cells. We evaluated cell migration, invasion, and the expression of associated proteins in SiHa, HaCaT-16E6, and HaCaT-16E7 cells using various assays. Results: Transcriptome analysis revealed pathways associated with proliferation/apoptosis (TNF-α signaling, UV radiation response, mitotic spindle formation, G2/M cell cycle, UPR, and IL-6/JAK/STAT), cellular metabolism (oxidative phosphorylation), and cell migration (angiogenesis, EMT, and TGF-α signaling) in SiHa cells. Key differentially expressed genes included PTGS2 (pro/antitumor), FOSL1, TNFRSF9, IL1B, DIO2, and PHLDA1 (antitumor), along with under-expressed genes with pro-tumor effects that may inhibit proliferation. Additionally, DKK1 overexpression suggested inhibition of cell migration. G-1 increased vimentin expression in SiHa cells and reduced it in HaCaT-16E6 and HaCaT-16E7 cells. However, G-1 did not affect α-SMA expression or cell migration in any of the cell lines but increased invasion in HaCaT-16E7 cells. Conclusions: GPER is a promising prognostic marker due to its ability to activate apoptosis and inhibit proliferation without promoting migration/invasion in CC cells. G-1 could potentially be a tool in the treatment of this neoplasia. [ABSTRACT FROM AUTHOR]

Sevoflurane is shown to curtail lung cancer (LC) development. Herein, this research sought to investigate the underlying mechanism of sevoflurane in regard to its repressive effects on LC. Expression levels of microRNA (miR)-153-3p, HIF1α, and KDM2B in LC tissues and cells were determined with qRT-PCR. Following sevoflurane pretreatment and/or ectopic expression and knockdown experiments, the malignant phenotypes, and levels of miR-153-3p, HIF1α, and KDM2B in LC A549 cells were detected using Transwell, scratch, EdU, CCK-8, Western blot, and qRT-PCR assays. Relationship between HIF1α and miR-153-3p was verified with a dual-luciferase reporter assay. The interaction between HIF1α and KDM2B was verified with a ChIP assay. LC tissues and cells presented low miR-153-3p expression and high HIF1α and KDM2B expression. Sevoflurane pretreatment, miR-153-3p upregulation, HIF1α downregulation, or KDM2B downregulation impeded the malignant phenotypes of A549 cells. Sevoflurane pretreatment augmented miR-153-3p expression, while miR-153-3p negatively targeted HIF1α. HIF1α bound to the KDM2B promoter to upregulate KDM2B. HIF1α or KDM2B overexpression counteracted the inhibitory effects of sevoflurane pretreatment on A549 cell malignant behaviors. Sevoflurane decreased HIF1α expression through upregulation of miR-153-3p, thereby reducing KDM2B transcription to restrict the malignant phenotypes of LC A549 cells. [ABSTRACT FROM AUTHOR]

This article engages with the debate about the causes for Russia's full-scale military invasion in Ukraine. The existing explanations are organized into three groups revolving around commonalities in their basic assumptions and causal arguments: geopolitics, civilisational choice, and dead-end capitalist transition. The aim is not to advance any theory in particular but to facilitate theory-building in general by identifying intellectual shortcuts and unresolved contradictions in all groups of explanations. The categorization cuts across disciplinary divisions and theoretical camps to propose a typology of arguments that can facilitate the development of better explanations for the invasion. This is relevant not only for the heuristic value of theorisations, but also for ensuring that the conditions precipitating the invasion are not reproduced in the post-war order. [ABSTRACT FROM AUTHOR]

Purpose: Thoracoscopic procedures such as video-assisted thoracoscopic surgery (VATS) and robot-assisted thoracoscopic surgery (RATS) have gained popularity for the treatment of thymoma. Accurate preoperative assessments of tumor invasion are crucial to identifying the appropriate surgical approach. Although imaging techniques have been used to predict invasion, a quantifiable method is still needed in clinical practice. Methods: The ubjects of this retrospective study were 226 patients with thymoma who underwent surgery at our hospital. Clinicopathological data, tumor staging, and recurrence rates were analyzed. Calcification identified through computed tomography (CT) defined the "calcified group" as having a long diameter of ≥ 5 mm. Statistical analyses were performed to assess relationships and survival outcomes. Results: The calcified group had higher Masaoka and World Health Organization classification than the noncalcified group, with significantly higher organ invasion rates. The calcified group also had remarkably higher recurrence rates. Conclusion: Thymoma calcification appears to correlate with increased invasiveness and recurrence rates, suggesting its potential as a predictor of tumor stage and prognosis. Despite its retrospective nature and inherent limitations, this study highlights the potential clinical significance of calcification in the surgical planning and prognostication of patients with thymoma. [ABSTRACT FROM AUTHOR]

Biodiversity is declining worldwide due to anthropogenic impacts, especially noxious for freshwater ecosystems, considering their close relationship with human activities. Damming is one of the most harmful human impacts that leads to the loss of several riverine fish through habitat loss or change. Herein, we aimed to assess the relationship between the composition of fish assemblages in reservoirs and the availability of littoral habitats, and whether these patterns differ between native and non-native species. Fish assemblages of fifteen reservoirs from up to downstream the Paraíba do Sul river basin were evaluated. Habitat availability was more important for native than for non-native species, after controlling for the influence of reservoir features. Local drivers were crucial for the occurrence of non-native species which thrived in the absence of complex habitats. Macrophytes seemed to play two key but quite antagonistic roles for fish species. They were positively related to native small characids, probably acting as shelter against predation, but they were also related to hypoxic conditions in eutrophic reservoirs. These findings stress the importance of preserving or restoring physically complex habitats as beneficial for native fish species through providing grounds for feeding (catfishes on leaves) and recruitment (juveniles of characids in macrophytes banks). [ABSTRACT FROM AUTHOR]

Placental trophoblast dysfunction has been proved to be closely related to the pathogenesis of preeclampsia. Coronaryxin-like actin-binding protein 1C (CORO1C) plays an important role in cell proliferation, apoptosis, invasion, and signal transduction, but its involvement in trophoblast dysfunction and preeclampsia remains uncertain. The expression of CORO1C in placental tissues of preeclampsia (PE) pregnant women and pregnant mice PE model were detected by real-time quantitative polymerase chain reaction (RT-qPCR), western blotting (WB) and immunohistochemical (IHC) staining. Next, the proliferation, invasion, migration and apoptosis were performed to explore the functions of CORO1C in HTR8/SVneo cell. Furthermore, the expression of CORO1C were detected in lncMALAT1 knockdown and overexpression HTR-8/SVneo cell. And then we investigated the possible regulatory mechanism of lncMALAT1 on CORO1C through bioinformatics analysis, FISH assays, RIP assays, RNA pull down and dual luciferase reporter assays. Finally, we further validated that lncMALAT1 regulate the function of placental trophoblast cells through CORO1C. The expression of CORO1C was significantly decreased in the placenta of PE patients and mice model, and positively associated with neonatal birth weight. And we found that CORO1C inhibited trophoblast proliferation, migration and invasion. Furthermore, reduced expression of lncMALAT1 impaired CORO1C level, thereby resulting in trophoblast dysfunction. Mechanistically, the dysregulation of lncMALAT1 promoted the expression of miR-133a-3p, strongly enhancing its binding to the 3′UTR region of CORO1C mRNA for degradation. This study demonstrated that the dysregulation of CORO1C via lncMALAT1/miR-133a-3p axis impairs trophoblast function and contributes to preeclampsia pathogenesis, providing novel insights in PE therapy through modulating CORO1C level. • The expression of CORO1C was downregulated in PE placenta. • Loss of CORO1C leads to defective proliferation, migration, invasion, and elevated apoptosis in placental trophoblasts. • LncMALAT1 positively regulates CORO1C expression by sponging miR133a-3p. • LncMALAT1 modulates placental trophoblast function through a CORO1C-dependent manner. [ABSTRACT FROM AUTHOR]

Hypopharyngeal squamous cell carcinoma (HSCC) is a highly invasive and fatal tumor with a poor prognosis in head and neck tumors. It is urgent to further study the molecular mechanism of HSCC progression and identify new effective therapeutic targets. Cell division cycle-related protein 3 (CDCA3) was reported overexpressed in several cancers and involved in tumor progression. However, the biological role of CDCA3 and its potential mechanism in HSCC remain undetermined. Reverse transcription quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry were used to detect the expression levels of CDCA3 in HSCC tissue and matched peritumoral tissue. The effects of CDCA3 on cell proliferation, invasion, and migration were explored using the Celigo image cytometry assay, MTT assay, flow cytometric analysis, cell invasion, and migration assays. The results showed that CDCA3 was upregulated in HSCC tissue and FaDu cell line. Knockdown of CDCA3 inhibited the proliferation, invasion, and migration of FaDu cells and promoted apoptosis of FaDu cells. Furthermore, knockdown of CDCA3 blocked the cell cycle in the G0/G1 phase. Mechanistically, CDCA3 may play a role in tumor progression of HSCC through the Akt/mTOR signaling pathway. In summary, these results suggest that CDCA3 serves as an oncogene in HSCC and may be used as a prognostic indicator and a potential therapeutic target for HSCC. [ABSTRACT FROM AUTHOR]

Temporal community stability, here defined as temporal mean divided by temporal SD, plays an important role in predicting certain ecosystem services. However, temporal stability can change with invasion, with greater abundances of invasive species potentially having greater impacts on native community stability. The exact consequences of invasion for temporal stability are unclear and, in part, depend on the particular metric of stability measured. In rangeland ecosystems, predicable forage is important for livestock production but can be threatened by invasion. Therefore, using an observational field study conducted over three years in Wyoming, we assessed which metrics of plant community stability were altered by invasion and whether those effects were mediated by two environmental variables (light and soil moisture). Bromus arvensis and Bromus tectorum are two invasive annual weeds found across US rangelands, including the northern mixed‐grass prairies of Wyoming. We established plots along natural invasion blocks of B. arvensis and B. tectorum abundance and collected plant species composition data over three growing seasons. We tested associations between seven different metrics of plant community stability and invasion by B. arvensis and B. tectorum. We found that species turnover increases with invasion by both species, while stability of forb (both brome species), C4 grass (B. arvensis only), and C3 grass (B. tectorum only) cover decreases with invasion. All metrics of stability associated with invasion supported the hypothesis of a destabilizing effect of invasion on the native plant community. Further, we found that light and soil moisture did mediate some associations between stability and invasion. Overall, our results align with previous work suggesting that invasive annual bromes can lead to decreased native plant stability, which has important implications for forage production and, thus, food security. [ABSTRACT FROM AUTHOR]

Background: Diseases of veterinary importance, such as bovine Anaplasmosis, cause significant economic losses. Due to this, the study of various proteins of the causal agent Anaplasma marginale has focused on surface proteins. However, a vaccine for this disease is not yet available. To this end, in this work, moonlighting proteins (MLPs) are presented as an alternative approach for the design of immunogens against A. marginale. Methods: The proteins of the strain MEX-15-099-01 were analyzed, and its MLPs were identified. Subsequently, four virulence-associated MLP genes were selected and identified using PCR. The proteins were analyzed using a structural homology approach and the collection of B-cell epitopes was predicted for each MLP. Finally, a pair of AmEno peptides were synthesized and the antigenic potential was tested using an iELISA. Results: Our bioinformatics analysis revealed the potential of AmEno, AmGroEl, AmEF-Tu, and AmDnaK proteins as promising candidates for designing immunogens. The PCR allowed the gene sequence identification in the genome of the strain MEX-15-099-01. Notably, AmEno-derived synthetic peptides showed antigenicity in an ELISA. Conclusions: Our study has shed light on the potential use of MLPs for immunogen design, demonstrating the antigenic potential of AmEno. [ABSTRACT FROM AUTHOR]

Fish hybridization is common in aquaculture worldwide, including in Brazil, with cross‐breeding between species of the genera Piaractus and Colossoma taking the lead. However, little is known about the genetic damage caused by hybrids that escape into natural environments. In the upper Paraná River region, hybrid fishes are overproduced; therefore, the use of molecular techniques for their monitoring and identification is necessary. This study aimed to detect the presence of possible hybridization between Piaractus and Colossoma in the upper Paraná River using the molecular markers cytochrome c oxidase subunit 1 (COI) and α‐tropomyosin (TROP). Fragments from 53 fish samples were analysed, and 41 samples were considered hybrids, with 12 confirmed pure, six as Piaractus mesopotamicus (pacu) and six as Piaractus brachypomus (pirapitinga). This is the first record of P. brachypomus, which is an invasive species in this basin, while Colossoma macropomum has not been observed. Molecular markers efficiently detected hybrids in the Ivinhema and Paraná rivers. The results showed a predominance of hybrid specimens from P. mesopotamicus × P. brachypomus. Our study suggests that more restrictions on hybridization and better supervision of fish farms are needed to prevent the escape of hybrids and the consequent ecological and genetic damage to native populations. We warn of the risk of a decline in the population of P. mesopotamicus, as this species is of great importance for fishing and maintaining the ecosystem. [ABSTRACT FROM AUTHOR]

Most human papillomavirus (HPV) types, including HPV16 and HPV18, are closely related to the occurrence of cervical cancer, predominantly through the action of viral oncoproteins E6 and E7. Curcumin, the active ingredient of the turmeric plant, has been gaining attention over the past two decades as an antioxidant, anti‐inflammatory, and anticancer agent. In the present study, the HPV‐positive cervical cancer cells HeLa and CaSki were treated with curcumin, and the results showed that curcumin has a dose‐dependent and time‐dependent inhibitory effect on cell viability. In addition, apoptosis induction was further quantitatively confirmed through flow cytometric analysis. Furthermore, the influence of different concentrations of curcumin on the mitochondrial membrane potential was evaluated through JC‐1 staining and found to dramatically decrease the membrane potential in treated HeLa and CaSki cells, suggesting the critical role of the mitochondrial pathway in their apoptosis‐inducing effect. This study also demonstrated the wound‐healing potential of curcumin, and the results of transwell assays showed that curcumin treatment inhibited HeLa and CaSki cell invasion and migration in a dose‐dependent manner compared with the control treatment. Curcumin also downregulated the expression of Bcl‐2, N‐cadherin, and Vimentin and upregulated the expression of Bax, C‐caspase‐3, and E‐cadherin in both cell lines. Further research showed that curcumin also selectively inhibited the expression of the viral oncoproteins E6 and E7, as demonstrated by western blot analysis; moreover, the downregulation of E6 was more significant than that of E7. Our research also showed that coculture with cells infected with siE6 lentivirus (siE6 cells) can inhibit the proliferation, invasion, and metastasis of HPV‐positive cells. While the siE6 cells were also treated with curcumin, the effect of curcumin monotherapy was offset. In summary, our research shows that curcumin regulates the apoptosis, migration, and invasion of cervical cancer cells, and the mechanism may be related to its ability to downregulate E6. This study provides a foundation for future research on the prevention and treatment of cervical cancer. [ABSTRACT FROM AUTHOR]

Understanding the mechanisms by which cancer cells switch between different adaptive states and evade therapeutic interventions is essential for clinical management. In this study, the in vivo cellular dynamics of a new chronic myeloid leukaemia cell line displaying altered phenotype and resistance to tyrosine kinase inhibitors were investigated in correlation with their parental cells for invasiveness/metastasis, angiogenic potential and population kinetics. We showed that the cells exhibiting drug resistance and plastic phenotype possess an increased capacity for invasion compared to their parental cells, that exposure to imatinib mesylate has the potential to enhance cellular motility and that in a leukaemic cell population, even a minority of plastic cells exhibit improved migratory ability. Furthermore, we show that these plastic cells have angiogenic and extravasation potential. The present study provides significant insights into the cellular dynamics displayed by a TKI‐resistant, phenotypically plastic CML cell line, using a zebrafish (Danio rerio) xenograft model. [ABSTRACT FROM AUTHOR]

This study has examined the linguistic differences in news reports published by Reuters and TASS on four distinct incidents during the 2022 Russia-Ukraine war. Employing discourse analysis as the methodological approach and discourse theory as the theoretical framework, the study has revealed significant linguistic and rhetorical disparities between the two media outlets, highlighting divergent ideological stances and power dynamics. The study has found that Reuters and TASS have employed distinct linguistic strategies that shape public ideologies and perceptions. TASS has portrayed the war from a Russian perspective, referring to it as a "special military operation" while excluding Ukrainian viewpoints. In contrast, Reuters has depicted the war as a full-scale invasion and emphasized allegations of war crimes while also excluding Russian viewpoints. Discrepancies have also emerged in reporting casualties and territorial control, with TASS and Reuters presenting conflicting figures and narratives. Neither outlet has cross-checked information, undermining their objectivity and contributing to biased reporting. The study underscores how the language used by TASS and Reuters serves to legitimize their respective positions and influence public perception, reflecting broader geopolitical power dynamics. Both media agencies have produced misleading narratives by relying solely on official statements from both nations without independent verification. [ABSTRACT FROM AUTHOR]

The malignant behavior and immune escape ability of cancer cells lead to therapeutic failure and poor prognosis for patients with various cancers, including colon cancer. Plexin domain containing 1 (PLXDC1) was initially identified to exert key roles in tumor by regulating angiogenesis and has recently proved to be involved in cell proliferation and migration of glioblastoma and gastric cancer cells. However, its roles in colon cancer remain unclear. In this study, the online bioinformatics databases confirmed high expression of PLXDC1 in colon cancer specimens, which was associated with cancer stages and nodal metastasis. Similarly, the increased expression of PLXDC1 was also validated in our collected samples and colon cancer cells. Moreover, patients with high expression of PLXDC1 had shorter survival, indicating that PLXDC1 might be a potential prognostic predictor for colon cancer patients. Notably, targeting PLXDC1 inhibited cancer cell viability and invasion, and enhanced cell apoptosis. Intriguingly, Tumor Immune Estimation Resource database confirmed that PLXDC1 expression was related to various tumor‐infiltrating immune cells in colon adenocarcinoma including macrophages, and its expression was also correlated with M2‐like macrophage markers. In vitro, colon cancer cells with PLXDC1 downregulation had a reduced ability to recruit and polarize macrophage towards M2 phenotype by decreasing the percentage of CD206+ cells and M2‐like markers (CD206, CD163, arginase1, and interleukin 10 [IL‐10]). Moreover, PLXDC1 knockdown attenuated M2 macrophage‐mediated promotion in cancer cell viability and invasion. Mechanically, inhibition of PLXDC1 suppressed activation of the IL‐6/Signal transducer and activator of transcription 3 (STAT3) signaling. Reactivating the above pathway by transfection with IL‐6 plasmids reversed the suppressive effects of PLXDC1 knockdown on cancer cell malignant behaviors, macrophage recruitment and M2‐like polarization. Thus, PLXDC1 downregulation may inhibit the malignancy of colon cancer cells and their ability to recruit and polarize macrophages towards M2 phenotype by blocking the IL‐6/STAT3 pathway. Together, targeting PLXDC1 may attenuate the progression of colon cancer by direct roles in cancer cells and indirect roles in macrophage polarization, representing a promising therapeutic target for colon cancer patients. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the effect of an isocitrate dehydrogenase 1 (IDH1) mutation (mutIDH1) on the invasion and angiogenesis of human glioma cells. Methods: Doxycycline was used to induce the expression of mutIDH1 in glioma cells. Transwell and wound healing assays were conducted to assess glioma cell migration and invasion. Western blotting and cell immunofluorescence were used to measure the expression levels of various proteins. The influence of bone morphogenetic protein 2 (BMP2) on invasion, angiogenesis-related factors, BMP2-related receptor expression, and changes in Smad signaling pathway-related proteins were evaluated after treatment with BMP2. Differential gene expression and reference transcription analysis were performed. Results: Successful infection with recombinant lentivirus expressing mutIDH1 was demonstrated. The IDH1 mutation promoted glioma cell migration and invasion while positively regulating the expression of vascularization-related factors and BMP2-related receptors. BMP2 exhibited a positive regulatory effect on the migration, invasion, and angiogenesis of mutIDH1-glioma cells, possibly mediated by BMP2-induced alterations in Smad signaling pathway-related factors.After BMP2 treatment, the differential genes of MutIDH1-glioma cells are closely related to the regulation of cell migration and cell adhesion, especially the regulation of Smad-related proteins. KEGG analysis confirmed that it was related to BMP signaling pathway and TGF-β signaling pathway and cell adhesion. Enrichment analysis of gene ontology and genome encyclopedia further confirmed the correlation of these pathways. Conclusion: Mutation of isocitrate dehydrogenase 1 promotes the migration, invasion, and angiogenesis of glioma cells, through its effects on the BMP2-driven Smad signaling pathway. In addition, BMP2 altered the transcriptional patterns of mutIDH1 glioma cells, enriching different gene loci in pathways associated with invasion, migration, and angiogenesis. [ABSTRACT FROM AUTHOR]

Backgrounds: Glioblastoma (GBM) is a highly aggressive brain cancer associated with poor prognosis, primarily attributed to its profound invasive characteristics. Glutamate is the main cause of invasion, and invasion is promoted by system Xc− (cystine/glutamate antiporter), which is highly expressed in GBM. To date, no studies have examined the relationship between invasion and the specific downregulation of system Xc− (xCT or SLC7A11) using shRNA in GBM. Objective: We aimed to determine the effect of a specific knockdown system, Xc−, in GBM using short hairpin RNA (shRNA) rather than pharmacological approaches. Results: Invasion was inhibited in GBM cells treated with sulfasalazine, a system Xc− inhibitor. Our experiments validated a reduction in extracellular glutamate concentration following sulfasalazine treatment, without affecting GBM proliferation or calcium response. However, the efficacy of pharmacological methods is hindered by nonspecific effects and the prevalence of multiple side effects. Therefore, we specifically targeted the system Xc− molecule through shRNA. Downregulation using shRNA demonstrated decreased invasion and extracellular glutamate levels, without affecting the calcium response and proliferation. Conclusion: The targeted inhibition of system Xc− using shRNA yields a notable reduction in GBM invasion. [ABSTRACT FROM AUTHOR]

Background: Bladder cancer (BC) originating from the bladder mucosa is a malignant tumor of the genitourinary system. Long non-coding RNAs (lncRNAs) can participate in cell proliferation and differentiation at multiple levels, and lncRNA dysregulation involves in the processes of malignant tumors. Methods: Focused on lncRNA small nucleolar RNA host gene 12 (SNHG12) and its target miR-143-3p, the specific mechanism related to BC was discovered. SNHG12 and miR-143-3p expression in BC samples was checked, together with the association with the malignant activities of BC cells. Results: As texted, SNHG12 expression went upward and miR-143-3p expression went downward in BC. SNHG12 depletion or miR-143-3p over-expression was causal for the suppression of BC cell activities. SNHG12 expression was directly associated with miR-143-3p expression. Ablating miR-143-3p abrogated changes in BC cell function induced by SNHG12 depletion. Conclusions: Generally, SNHG12/miR-143-3p induces the malignant activities of BC cells. [ABSTRACT FROM AUTHOR]

Background aim Methods Results Conclusions Breast cancer is a prevalent and aggressive malignancy associated with elevated mortality rates worldwide. Dysregulation of the c‐MYC oncogene and aberrant activation of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) signaling pathway are common features in breast cancer progression, rendering them attractive therapeutic targets. Here, we assessed the effects of the plant derivative, xanthine, on breast cancer cells and explored the molecular mechanisms underlying its activity.Breast cancer cell lines were treated with xanthine, followed by assessment of c‐MYC expression levels. Cell proliferation, invasion, and migration were analyzed to assess the effects of xanthine treatment on breast cancer cell behavior.Xanthine treatment induced a decrease in c‐MYC expression, resulting in significant inhibition of breast cancer cell proliferation, invasion, and migration. Mechanistic investigations revealed that these effects were mediated by suppression of the PI3K/AKT signaling pathway.Xanthine shows great potential for breast cancer treatment by targeting c‐MYC via the PI3K/AKT signaling pathway. Our findings indicate that development of xanthine as a novel treatment option for breast cancer, which acts by influencing key oncogenic pathways involved in tumor progression, may be warranted. [ABSTRACT FROM AUTHOR]

Preeclampsia is a pregnancy-specific disorder characterized by de novo development of hypertension and proteinuria over 20 weeks gestation that has been associated with the dysfunction of trophoblasts. Current evidence suggests that syncytin-1 plays an important role in the non-fusogenic biological activity of trophoblasts, except for specific fusogenic function. However, the underlying mechanism remains unclear. The expression and location of syncytin-1 in normal and the late-onset preeclampsia placentas were detected by quantitative real-time PCR, western blotting and immunofluorescence. Morphological and apoptosis analysis were processed in placentas. The ex vivo extravillous explant culture model was used to explore the effect of syncytin-1 on EVT outgrowths. Real-time quantitative PCR and immunoblotting were used to calculate syncytin-1 levels in the trophoblast cells before and after syncytin-1 knockdown or overexpression. CCK-8 assay was used to detect the cell viability. TUNEL staining and immunoblotting were processed in trophoblast cells. Transwell assays and wound healing assays were utilize to assess the invasion and migration of trophoblastic cells. Conditional knockout of syncytin-a mouse model was conducted to present the change of placentas in vivo. The ex vivo extravillous explant culture model was used to explore the effect of syncytin-1 on EVT outgrowths. Western blotting was used to identify the key proteins of PI3K/Akt pathways and invasion-related proteins in trophoblast cells. Here, reduced syncytin-1 was identified in the late-onset preeclampsia placentas. Reduced syncytin-1 may attenuates the EMT process by promoting apoptosis, inhibiting proliferation and invasion by suppressed PI3K/Akt pathway in trophoblast cells. Our findings provide novel insights into the non-fusogenic biological function of reduced syncytin-1 that may be involves in the pathogenesis of preeclampsia. • Reduced syncytin-1 inhibited trophoblast cells function • Which may be involved in the pathogenesis of preeclampsia. [ABSTRACT FROM AUTHOR]

Non-coding RNAs (ncRNAs), which are usually considered not to encode proteins, are widely involved in important activities including signal transduction and cell proliferation. However, recent studies have shown that small peptides encoded by ncRNAs (SPENs) have important roles in the development of malignant tumors. Some SPENs participate in the regulation of skeleton reorganization, intercellular adhesion, signaling and other processes of tumor cells, with effects on the invasive and migratory abilities of the cells. Therefore, SPENs have potential applications as therapeutic targets and biomarkers of malignant tumors. Invasion and migration of malignant tumor cells are themain reasons for poor prognosis of cancer patients and represent the most challenging aspects of treatment of malignant tumors. Currently, the main treatments for tumors include surgery, radiotherapy, targeted drug therapy. Surgery, however, is reserved for early stages of cancer and carries risks and costs. Radiotherapy and targeted therapy have serious side effects. This review describes the mechanisms of SPENs and their roles in tumor invasion and migration,with the aimof providing newtargets for tumor diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Alpha beta hydrolase domain containing 5 (ABHD5) is an essential coactivator of adipose triglyceride lipase (ATGL), a rate-limiting enzyme in various cell types that promotes the hydrolysis of triacylglycerol (TG) into diacylglycerol (DG) and fatty acid (FA). It acts as a critical regulatory factor in cellular lipid metabolism. The reprogramming of lipid metabolism is one of the hallmarks of cancer, suggesting that altering lipid metabolism could become a new strategy for tumor treatment. Research has revealed a close association between ABHD5 and the development and progression of malignancies. This review summarizes the role of ABHD5 in various malignant tumors and explores the different signaling pathways and metabolic routes that may be involved, providing a comprehensive mechanistic understanding of ABHD5. [ABSTRACT FROM AUTHOR]

Introduction: Tongue squamous cell carcinoma (TSCC) is a common malignant tumour type with aggressive invasion and a poor prognosis. To date, invasion-related gene expression signatures for the prognostic stratification of TSCC patients are unavailable in clinical practice. This study aimed to assess the impact of invasion-related genes on the prognosis of TSCC patients. Methods: We obtained mRNA profiles and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases (TCGA-TSCC and GSE41116, respectively). The TSCC samples from the TCGA-TSCC cohort were randomly divided into TCGA training and TCGA test datasets at a 7:3 ratio. Next, a disease-free survival (DFS) prognostic risk model was established on the basis of univariate and stepwise multivariate Cox regression analyses of the TCGA training cohort. Moreover, prognostic genes were screened. The model was subsequently evaluated and validated using the TCGA test and GSE41116 datasets. In addition, the prognostic genes were validated in the human TSCC cell line UM1 and the human oral keratinocyte (HOK) cell line using quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Results: A total of 70 candidate genes related to invasion were identified in the TCGA-TSCC cohort. DFS data were subsequently constructed, and 6 prognostic genes, HMGN2, MYL12B, ACTB, PPP1CA, PSMB9, and IFITM3, were identified. The TSCC samples were divided into high- and low-risk groups in the TCGA training, TCGA test, and GSE41116 cohorts, respectively. In particular, patients with TSCC in the low-risk group had longer DFS than those in the high-risk group. Furthermore, qRT-PCR analysis confirmed that the expression levels of the 6 prognostic genes were significantly greater in the TSCC cell line UM1 than in the HOK cell line. Conclusion: This study identified new invasion-related target genes related to poor prognosis in TSCC patients, providing new insights into the underlying mechanisms of TSCC invasion. [ABSTRACT FROM AUTHOR]

Galectins are a class of lectins that are extensively expressed in all organisms. Galectins are involved in a range of functions, including early development, tissue regeneration, cancer and inflammation. It has been shown that galectin-8 is expressed in the villous and extravillous trophoblast (EVT) cells of the human placenta; however, its physiological role in pregnancy establishment has not been elucidated. Taking these factors into account, we investigated the functional role of galectin-8 in HTR-8/SVneo cells—a human EVT cell line—and human primary cytotrophoblast cells isolated from a first-trimester placenta. We analyzed the effects of recombinant human galectin-8 (rh galectin-8) on the adhesion, migration and invasion of HTR-8/SVneo cells. We used qPCR, cell-based ELISA (cELISA) and gelatin zymography to study the effects of galectin-8 on mediators of these processes, such as integrin subunits alpha-1 and beta-1 and matrix metalloproteinases (MMPs)-2 and -9, on the mRNA and protein levels. Further, we studied the effects of galectin-8 on primary cytotrophoblast cells' invasion. Galectin-8 stimulated the adhesion, migration and invasion of HTR-8/SVneo cells, as well as the invasion of primary cytotrophoblasts. In addition, the MMP-2 and -9 levels were increased, while the expression of integrins alpha-1 and beta-1 was not affected. Galectin-8 has the ability to positively affect EVTs' invasion, so it can be considered a significant factor in the trophoblast cell invasion process. [ABSTRACT FROM AUTHOR]

Meningiomas are predominantly benign tumors, but there are also malignant forms that are associated with a poor prognosis. Like almost all tumors, meningiomas metabolize glucose as part of aerobic glycolysis (Warburg effect) for energy supply, so there are attempts to influence the prognosis of tumor diseases using a glucose-reduced diet. This altered metabolism leads to so called hallmarks of cancer, such as glycation and glycosylation. In this study, we investigated the influence of low (3 mM), normal (5.5 mM) and high glucose (15 mM) on a malignant meningioma cell line (IOMM-Lee, WHO grade 3). In addition, the influence of methylglyoxal, a by-product of glycolysis and a precursor for glycation, was investigated. Impedance-based methods (ECIS and RTCA) were used to study migration and invasion, and immunoblotting was used to analyze the expression of proteins relevant to these processes, such as focal adhesion kinase (FAK), merlin or integrin ß1. We were able to show that low glucose reduced the invasive potential of the cells, which was associated with a reduced amount of sialic acid. Under high glucose, barrier function was impaired and adhesion decreased, which correlated with a decreased expression of FAK. [ABSTRACT FROM AUTHOR]

We previously described a novel Plasmodium vivax invasion mechanism into human reticulocytes via the PvRBP2a-CD98 receptor-ligand pair. Using linear epitope mapping, we assessed the PvRBP2a epitopes involved in CD98 binding and recognized by antibodies from patients who were infected. We identified 2 epitope clusters mediating PvRBP2a-CD98 interaction. Cluster B (PvRBP2a431-448, TAALKEKGKLLANLYNKL) was the target of antibody responses in humans infected by P vivax. Peptides from each cluster were able to prevent live parasite invasion of human reticulocytes. These results provide new insights for development of a malaria blood-stage vaccine against P vivax. [ABSTRACT FROM AUTHOR]

There is extensive peripheral nerve infiltration and tumor innervation in head and neck cancer, which promotes tumor progress and brings worse prognosis. Schwann cells (SCs) are a type of glial cells that are widely distributed in the peripheral nervous system and are involved in nerve injury repair. In recent years, more and more studies have shown that SCs play an important role in the tumor microenvironment (TME). Reprogrammed SCs promote peripheral nerve infiltration and tumor innervation through signal interaction with tumor and nerves on the one hand, and directly act on TME components and promote tumor progression on the other hand. This paper mainly discusses the cross-talk patterns of SCs and cancer-nerve signals, as well as the mechanism of action of SCS-related signals in TME, and explore potential targets for therapeutic intervention in SCS-related head and neck cancer. [ABSTRACT FROM AUTHOR]

Invasive growth is a critical process in tumor progression, requiring the activation of various molecular processes in tumor cells at the invasive front. Intercellular communication between heterogeneous tumor cells enhances cellular activation and adaptation to specific microenvironments. One mechanism of intercellular communication is the delivery of miRNAs through tumor cell-derived extracellular vesicles (EVs). In this context we have observed that conditioned media from a highly invasive cell subpopulation (BLM-HI) enhances the invasive capacity of the parental cell line (BLM). Therefore, we hypothesized that this complex change of cellular behavior is influenced by EV-transported miRNAs. The treatment of BLM cells with EVs derived from BLM-HI cells resulted in a significantly enhanced invasive capacity, as observed in Matrigel-embedded spheroids and in 2D Boyden chamber assays, with a dose-dependent effect. Conversely, the invasive capacity of BLM cells was reduced when secretion of EVs was inhibited by a sphingomyelinase inhibitor. To investigate the molecular mechanisms behind this effect, we performed next-generation sequencing and identified an enrichment of miR-1246 in these EVs. In functional analyses we demonstrated that both the EV mediated delivery of miR-1246 as well as overexpression contributes to the enhanced invasiveness of BLM cells. We identified a binding site of miR-1246 in the 3'UTR of cyclin G2 (CCNG2) and demonstrated direct binding by a luciferase reporter assay. Increased expression of CCNG2 has been associated with cancer metastasis and poor patient outcomes in other malignancies. Our study demonstrates that intercellular communication contributes to the transfer of properties, such as increased invasive capacity, between heterogeneous melanoma cells via EV-transported miRNAs. [ABSTRACT FROM AUTHOR]

The functional role and molecular mechanisms of small‐nucleolar RNA host gene 14 (SNHG14) in triple‐negative breast cancer (TNBC) progression remain unclear. The expression levels of SNHG14 in breast cancer samples and cell lines were determined using real‐time quantitative polymerase chain reaction. Cell proliferation, migration, and invasion abilities were detected using MTS and transwell assays. By RNA sequencing, differentially expressed genes were identified between the SNHG14 siRNA and the negative control group. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to predict the targets and pathways regulated by SNHG14. pRAF, pMEK, and pERK expression were measured by western blot. The xenograft model was constructed to access the biological function of SNHG14 in vivo. A minimal patient‐derived xenograft model was established to evaluate the sensitivity to chemotherapy drugs. Our data indicated that SNHG14 expression was increased in TNBC tissues and cell lines. SNHG14 knockdown attenuated the proliferation, migration, and invasion abilities of TNBC cells both in vivo and in vitro. High SNHG14 expression was associated with lymph node metastasis and a high Ki67 index. The targets of SNHG14 were mainly enriched in the MAPK signaling pathway. pRAF, pMEK, and pERK expression were downregulated after being transfected with SNHG14 siRNA. Compared with the negative control group, the expression of CACNA1I, DUSP8, FGF17, FGFR4, FOS, PDGFRB, and DDIT3 was increased, and the expression of MKNK1 was decreased in the SNHG14 siRNA group. Minimal patient‐derived xenograft model demonstrated that knockdown of SNHG14 enhanced the sensitivity to Docetaxel in vivo. Compared with the DMSO group, the proliferation of Docetaxel‐resistant MDA‐MB‐231 cells was decreased in Dabrafenib, PD184352, and FR180204 treatment groups. SNHG14 knockdown inhibits TNBC progression by regulating the ERK/MAPK signaling pathway, which provides evidence for SNHG14 as a potential target for TNBC therapy. [ABSTRACT FROM AUTHOR]