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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.

Background: Cholangiocarcinoma (CCA) is an aggressive malignancy with limited treatment options and poor prognosis. Platelet-Derived Growth Factor CC (PDGF-CC) has been implicated in the progression of various tumors, but its specific role in CCA is not well understood. This study aims to investigate the expression and function of PDGF-CC in CCA and evaluate its potential as a therapeutic target. Methods: We conducted gene expression analysis using the GEPIA database to compare PDGF-CC mRNA levels in CCA tissues and normal tissues. Serum samples from CCA patients were analyzed for PDGF-CC protein levels, and immunohistochemistry was used to assess PDGF-CC expression in tissue samples. The impact of PDGF-CC on CCA cell behavior was examined by knocking out PDGF-CC in HuCCT1 and QBC939 cell lines, followed by assessments of cell proliferation, migration, invasion, and colony formation in vitro. Additionally, the effects of PDGF-CC knockout were evaluated in xenograft models. The therapeutic potential of PDGF-CC inhibition was further explored using pharmacological inhibitors and antibodies. Results: PDGF-CC mRNA and protein levels were significantly elevated in CCA tissues and patient sera compared to normal controls. Immunohistochemical analysis confirmed increased PDGF-CC expression in CCA tissues. High PDGF-CC expression correlated with poor overall survival in CCA patients, as shown by Kaplan-Meier analysis. Functional assays revealed that PDGF-CC knockout significantly reduced proliferation, migration, invasion, and colony formation in HuCCT1 and QBC939 cells, the lines with the highest PDGF-CC levels. In vivo, PDGF-CC knockout markedly decreased tumor growth in xenograft models. Pharmacological inhibition of PDGF-CC mirrored the effects of genetic knockout, suggesting it as a viable therapeutic strategy. Conclusions: This study underscores the critical role of PDGF-CC in CCA progression and supports the potential of PDGF-CC inhibitors as a therapeutic approach. Given the association between high PDGF-CC expression and poor prognosis, targeting PDGF-CC may improve outcomes for CCA patients. Further clinical investigations are warranted to develop PDGF-CC-targeted therapies for CCA. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic and lethal disease. Gasdermins are primarily associated with necrosis via membrane permeabilization and pyroptosis, a lytic pro‐inflammatory type of cell death. In this study, GSDMC upregulation during PDAC progression is reported. GSDMC directly induces genes related to stemness, EMT, and immune evasion. Targeting Gsdmc in murine PDAC models reprograms the immunosuppressive tumor microenvironment, rescuing the recruitment of anti‐tumor immune cells through CXCL9. This not only results in diminished tumor initiation, growth and metastasis, but also enhances the response to KRASG12D inhibition and PD‐1 checkpoint blockade, respectively. Mechanistically, it is discovered that ADAM17 cleaves GSDMC, releasing nuclear fragments binding to promoter regions of stemness, metastasis, and immune evasion‐related genes. Pharmacological inhibition of GSDMC cleavage or prevention of its nuclear translocation is equally effective in suppressing GSDMC's downstream targets and inhibiting PDAC progression. The findings establish GSDMC as a potential therapeutic target for enhancing treatment response in this deadly disease. [ABSTRACT FROM AUTHOR]

Ecosystem exposure to a biological invasion such as plant invasion could contribute to the extinction of native species and loss of productivity and ecosystem balance. Solidago canadensis (S. canadensis) is a highly invasive species that has formed monocultures in China, Europe, Asia, Australia, and New Zealand. It was designated as a notorious invasive species by the Chinese government. It has adversely affected the agroecosystem's ability to germinate various plant seeds, including wheat, lettuce, and pepper, which could lead to food insecurity. This study was conducted to control the invasive species S. canadensis by utilizing a competitive species, Sorghum bicolor (S. bicolor) as a cover plant. Sorghum bicolor exudes allelochemicals such as sorgoleone from its roots which suppress the photosystem II activity of nearby plants. The synthesis of sorgoleone depends on a supply of nitrogen. The present study involved the cultivation of S. bicolor alongside the invasive species S. canadensis , with three different invasion levels (high, medium, and low) and three different nitrogen forms (ammonical, nitrate, and combined ammonical and nitrate nitrogen) applied as a modified Hogland solution. S. bicolor expressed higher performance over the invasive species under ammonical and combined nitrogen forms under low and medium invasion levels. Furthermore, even at greater levels of invasion, S. bicolor was not suppressed by S. canadensis. However, the plant height and dry biomass of S. bicolor were significantly high across both nitrogen forms. Leaf area, CO2 uptake, and photosystem II activity of S. canadensis were unable to sustain its growth under the low invasion condition. The plant biomass of S. canadensis was suppressed by up to 80% and the relative dominance index of S. bicolor was 5.22 over S. canadensis. There was a strong correlation between CO2 uptake, leaf area, and plant biomass. Principal component analysis showed that the first four components had a total variance of 96.89%, with principal component 1 (PC1) having the highest eigenvalue at 18.65. These promising findings suggested that S. bicolor , whose high intensity might be employed to control the invasion process for environmental safety, might be able to recover the barren ground that S. canadensis had invaded. [ABSTRACT FROM AUTHOR]

Patients with advanced and recurrent cervical cancer often lack satisfactory treatment outcomes. Thus, it is necessary to seek reliable biomarkers that provide the ability to identify the disease at an early stage and predict the patient prognosis, providing new strategies for the treatment of cervical cancer. The sequencing data of ITGA3 were retrieved from public datasets. Immune infiltration and sensitivity of potential immunotherapy and chemotherapy have been analyzed between two subgroups. Functional analysis was applied to excavate the related pathways of ITGA3 in cervical cancer. Furthermore, the impact of ITGA3 in tumor progression has been verified in vitro. The results revealed that the level of ITGA3 was upregulated in cervical cancer, and was positively correlated with worse prognosis. The tumor microenvironment of patients in the high-risk group was immunosuppressed. Patients in high-risk group may not benefit from immunotherapy, but be may be sensitive to several chemotherapy drugs. Notably, the angiogenesis, epithelial mesenchymal transition, and PI3K pathway were increased in high-risk group. Collectively, ITGA3 is a marker of poor prognosis and promotes tumor progression by regulating PI3K/AKT pathway in cervical cancer. Our results provide new insights for potential molecular targeted therapy and prognostic prediction of cervical cancer. [ABSTRACT FROM AUTHOR]

Background: Streptococcus canis is a commensal bacterium in companion animals. This microorganism can infect humans who have been in deep contact with or bitten by pet dogs, suggesting that the skin/soft tissue is one of infection entry sites. To understand pathological process in human cells, we aimed to determine S. canis transcriptomic changes in invasive environments of human keratinocytes. Methods: We selected one isolate from candidates with whole-genome sequences, based on re-obtained cell invasion ability (CIA) data into human keratinocytes along with bacterial cytotoxicity. RNA-sequencing was conducted for the samples at baselines and 2 h/5 hr post-inoculation using NovaSeq 6000. Global/differential gene expression analyses [principal component analysis (PCA)/k-means clustering analysis/differentially expressed gene (DEG) analyses] were performed. We classified DEGs into their functional categories. To validate transcriptomic results, we did quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays. Results: FU1 isolate was selected from seven candidates, based on re-obtained CIA data with less cytotoxicity. Total read bases of 6.17–9.02 Gbp were obtained by RNA-sequencing. PCA and k-means clustering analysis indicated clustering according to their inoculation times. Volcano plots and Venn diagrams revealed that S. canis invasion into keratinocytes produced altered distributions of many genes. Gene ontology enrichment analysis showed most of the gene expressions were downregulated. DEG functional analysis showed the downregulated DEGs belonging to energy production and conversion/carbohydrate transport and metabolism/amino acid transport and metabolism/nucleotide transport and metabolism, with the upregulated DEGs belonging to transcription. qRT-PCR assays for downregulated/upregulated expressions of four genes (pgk–slo/opuAA–kdpB) validated transcriptomic results. Conclusion: Our observations suggest that S. canis can downregulate its metabolism-associated gene expressions in human keratinocyte environments. The observed gene expression changes can imply the latent infection in human cells. Further investigation is needed to elucidate the underlying mechanisms for the latent infection. [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]

Background: Gastric cancer is one of the most common malignant tumors in the world, with a poor prognosis. HOXC is a family of transcription factors that are up-regulated in gastric cancer tissues. However, the relationship between Homeobox C12 (HOXC12) and gastric cancer is still unclear. Methods: TCGA-STAD and HPA data were analyzed to explore HOXC12 level. Kaplan–Meier Plotter was used to analyze the relationship between HOXC12 level and the prognosis of gastric cancer patients. The HOXC12 was knocked down or overexpressed by shRNA or overexpression vector to explore its functions. Cell migration/invasion assays and wound healing assay were used to assess the invasion/migration ability of gastric cancer cells. Western blot and qPCR were used to detect gene expression and the activation of Wnt/β-catenin signaling pathway. Dual-luciferase reporter assay was used to detect the active region bound by HOXC12 in the promoter of Spalt-like transcription factor 4 (SALL4). Results: HOXC12 was highly expressed in gastric cancer and was positively correlated with the poor prognosis of gastric cancer patients. HOXC12 promotes the invasion and migration of gastric cancer cells via Wnt/β-catenin signaling pathway. HOXC12 upregulated the transcription of SALL4 by binding to its promoter. HOXC12 was negatively correlated with both the levels of CD8+ T cells and T cell cytotoxicity-related genes. Conclusion: HOXC12 promotes the invasion/migration of gastric cancer cells via SALL4/Wnt/β-catenin axis, and is negatively correlated with the infiltration of CD8+ T cells, suggesting HOXC12 as a diagnostic marker and a potential therapeutic target for gastric cancer. [ABSTRACT FROM AUTHOR]

Nuclear protein‐1 (NUPR1) (also known as p8) is one of the genes associated with transcription factors that participate in various aspects of cancer initiation and development. However, the molecular mechanisms of NUPR1 in bladder cancer (BLCA) remain unclear. We conducted an analysis of the correlation between NUPR1 expression and related genes using the Gene Expression Omnibus (GEO) online database. We employed lentivirus‐mediated small interfering RNA (siRNA) to knockdown the expression of NUPR1 in two human BLCA cell lines. In vitro experiments were conducted to validate the impact of NUPR1 interference on BLCA and the influence of NUPR1 on the transcription of chemokine receptor‐2 (CCR2). Furthermore, transcription factors for CCR2 were predicted using the PROMO database. Co‐immunoprecipitation (Co‐IP) and immunofluorescence double staining were used to detect the binding between NUPR1 and CCAAT/enhancer binding protein γ (CEBPG). In vivo and in vitro experiments were conducted to validate that NUPR1 regulates CCR2 transcription through CEBPG. In vitro experiments indicate that the suppression of NUPR1 inhibited BLCA growth. Analysis of the GEO database revealed a positive correlation between the expression of NUPR1 and CCR2. Luciferase experiments confirmed that NUPR1 influences the transcription of CCR2. Online data indicates that CEBPG is a transcription factor for CCR2. Co‐IP and immunofluorescence double staining confirmed binding between NUPR1 and CEBPG. Luciferase assays and chromatin immunoprecipitation (ChIP) demonstrate that CEBPG regulates the transcription of CCR2. Additionally, rescue experiments at the cellular level and animal experiments validated the aforementioned mechanism. NUPR1 promotes a promotional role in BLCA, and interference with NUPR1 can inhibit the proliferation and invasive abilities of BLCA. There was a correlation between the expressions of NUPR1 and CCR2, and NUPR1 binds with CEBPG in the cell nucleus. Transcriptional regulation of CCR2 by NUPR1 may be achieved through the involvement of CEBPG. [ABSTRACT FROM AUTHOR]

Thrombin, a key enzyme in the regulation of hemostasis, has been implicated in cancer progression. This study explored the effect of recombinant tyrosine-sulfated haemathrin on cancer cell behavior and signaling pathways compared to wild-type (WT) haemathrin 2. The recombinant proteins, tyrosine-sulfated haemathrin 2 (haemathrin 2S), and WT haemathrin 2 were produced in Escherichia coli and subsequently purified and applied to SKOV3 and MDA-MB-231 cells with and without thrombin stimulation. Cell migration and invasion were assessed using wound healing and Transwell assays, respectively. Haemathrin 2S treatment significantly diminished cell migration and invasion promoted by thrombin in both SKOV3 and MDA-MB-231 cells (p < 0.05). Additionally, haemathrin 2S effectively inhibited thrombin-induced phosphorylation of serine/threonine kinase (Akt) in both cell lines (p < 0.05), while WT haemathrin 2 had this effect only in MDA-MB-231 cells. Furthermore, haemathrin 2S significantly reduced thrombin-activated phosphorylation of extracellular signal-regulated kinases (ERK) and p38 in both cell lines (p < 0.05) and reversed E/N-cadherin expression in thrombin-treated MDA-MB-231 cells (p < 0.05), which were not observed with WT haemathrin 2. Overall, haemathrin 2S was more effective than WT haemathrin 2 in reducing cancer cell migration and invasion, indicating that targeting thrombin with sulfated haemathrin is a promising strategy for cancer therapy. However, further in vivo studies are needed to confirm these results. [ABSTRACT FROM AUTHOR]

Kinin receptors B1 and B2 are involved in migration and invasion in gastric, glioma, and cervical cancer cells, among others. However, the role of kinin receptors in breast cancer cells has been poorly studied. We aimed to reveal the impact of B1 and B2 receptors on migration and invasion in breast cancer cells and demonstrate their capacity to modulate in vivo tumor growth. MDA-MB-231, MCF-7, and T47D cells treated with Lys-des[Arg9]bradykinin (LDBK) or bradykinin (BK) were used to evaluate migration and invasion. Des-[Arg9]-Leu8-BK and HOE-140 were used as antagonists for the B1 and B2 receptors. MDA-MB-231 cells incubated or not with antagonists were subcutaneously inoculated in BALBc NOD/SCID mice to evaluate tumor growth. LDBK and BK treatment significantly increased migration and invasion in breast cancer cells, effects that were negated when antagonists were used. The use of antagonists in vivo inhibited tumor growth. Moreover, the migration and invasion induced by kinins in breast cancer cells were inhibited when focal adhesion kinase (FAK) and Src inhibitors were used. The novelty revealed in our work is that B1 and B2 receptors activated by LDBK and BK induce migration and invasion in breast cancer cells via a mechanism that involves the FAK–Src signaling pathway, and the antagonism of both receptors in vivo impairs breast tumor growth. [ABSTRACT FROM AUTHOR]

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]

It has been evidenced that ROR2 influences the growth of many tumors, including non‐small cell lung cancer, osteosarcoma, and breast cancer. This research examined the effect of the WNT1/ROR2 signaling pathway on the progression of triple‐negative breast cancer (TNBC). Bioinformatics analysis results demonstrated that ROR2 had a higher messenger RNA (mRNA) expression level in TNBC tissues and was positively correlated with poor patient prognosis. Western blot analysis (WB) and quantitative reverse transcription polymerase chain reaction demonstrated that TNBC cells had relatively higher ROR2 mRNA and protein levels than normal cell lines. Transwell and Cell Counting Kit‐8 (CCK‐8) assay further proved that downregulating ROR2 expression dramatically slowed the MDA‐MB‐231 cell progression. WB detection of epithelial‐mesenchymal transition (EMT)‐related proteins suggested that knocking down ROR2 could alleviate the EMT tendency of cancer cells. The WNT1/ROR2 signaling pathway could be inhibited by the WNT inhibitor pyrvinium pamoate (PP). Experiments on in vitro cell functional recovery have demonstrated that PP could restore malignant phenotypes caused by ROR2 overexpression. Finally, the mouse model experiments further validated the anticancer effect of PP on TNBC. Generally speaking, the malignant progression of TNBC could be stimulated by the WNT1/ROR2 signaling pathway which can be inhibited by PP, suggesting the potential value of PP in controlling TNBC. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) ranks as the sixth most prevalent cancer worldwide. The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, contributing to increased malignancy. While Pleiotropic Regulator 1 (PLRG1) is upregulated in HCC and is associated with enhanced cell proliferation, its oncogenic role in EMT remains unclear. In this study, we demonstrate that PLRG1 promotes EMT in HCC cells. Knockdown of PLRG1 in Huh7 cells resulted in decreased expression of the EMT markers N-cadherin and Snail, and impaired cell migration and invasion. Chromatin immunoprecipitation (ChIP) and luciferase assays identified Y-box binding protein 1 (YBX1) as a direct regulator of PLRG1 transcription, binding to its promoter region. Overexpression of YBX1 in SNU-449 cells led to increased PLRG1 expression and subsequent EMT activation, as well as enhanced migration, and invasion. These effects were attenuated by PLRG1 knockdown. Our findings indicate that YBX1 drives EMT in HCC by upregulating PLRG1, offering novel insights into the molecular mechanisms underlying HCC progression. [ABSTRACT FROM AUTHOR]

BarH-like homeobox 2 (BARX2) has been identified to play a key role in the development of multiple cancers. Meanwhile, BARX2 may be an independent prognostic biomarker for patients suffering from hepatocellular carcinoma (HCC). Nevertheless, the regulatory role of BARX2 in HCC is still unclear and needs to be unveiled. In this study, the expressions of BARX2 and N-acetylgalactosaminyltransferase 4 (GALNT4) were evaluated by quantitative real-time PCR (qRT-PCR) as well as western blot. Besides, the abilities of cells to proliferate, migrate, invade, and angiogenesis were assessed with CCK-8, colony formation, wound-healing, Transwell, and tube formation assays, separately. Cell apoptosis was determined by flow cytometry analysis. The binding relationship between BARX2 and GALNT4 was predicted by JASPAR website and verified using Chromatin immunoprecipitation (ChIP) and luciferase report assay. It was discovered that BARX2 was reduced in HCC cell lines, while its overexpression greatly repressed cell proliferation, migration, invasion, and angiogenesis and promoted cell apoptosis in HuH7 and MHCC97-H cells. BARX2 could bind to GALNT4 promoter and positively regulate GALNT4 expression. In addition, GALNT4 deficiency partly abolished the inhibitory effects of BARX2 on the progression of HCC. In summary, this study highlights that BARX2 may hold promise for serving as a potential therapeutic target, facilitating the development of a novel therapeutic strategy against HCC. [ABSTRACT FROM AUTHOR]

Pancreatic cancer is a fatal malignancy typically diagnosed in older males and has an aggressive progression. The function of the miR-1180/FXYD5 axis in pancreatic cancer malignant behaviors was investigated. 20 pairs of pancreatic cancer and adjacent normal tissue samples were harvested from pancreatic cancer patients, and qRT-PCR, IHC, and western blot assays were performed, respectively, to detect the mRNA expression and protein levels of miR-1180 or FXYD5. Transwell and scratch assays were conducted to detect the migratory and invasive ability of pancreatic cancer cells; a Dual-luciferase reporter assay was employed to validate miR-1180 targeting FXYD5. miR-1180 targeting FXYD5 to regulate the migratory and invasive ability of pancreatic cancer cells was validated in mouse xenograft tumor models. FXYD5 expression was increased in pancreatic cancer tissue samples than in adjacent normal tissue samples (P < 0.01), and FXYD5 expression exhibited a positive correlation with the migratory and invasive ability of pancreatic cancer cells. miR-1180 targeted FXYD5 and negatively regulated FXYD5. Restoring miR-1180 expression could inhibit the migratory and invasive ability of pancreatic cancer cells (P < 0.01), and this effect could potentially be alleviated by FXYD5 overexpression. The miR-1180/FXYD5 axis positively regulated E-cadherin and negatively regulated MMP2 and MMP9 expression levels. In vivo findings demonstrated that miR-1180 overexpression inhibited tumor growth and lung metastasis (P < 0.05), while FXYD5 overexpression promoted tumor growth and lung metastasis (P < 0.05). In conclusion, the miR-1180 /FXYD5 axis could be involved in pancreatic cancer metastasis through the regulation of EMT and extracellular matrix degradation. [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]

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]

Purpose: Breast cancer brain metastasis (BCBM) is a deadly clinical problem, and the exact underlying mechanisms remain elusive. Junctional adhesion molecule (JAM), a tight junction protein, is a key negative regulator of cancer cell invasion and metastasis. Methods: Junction adhesion molecule 3 (JAM3) expression in breast cancer was analyzed using bioinformatics methods and confirmed by PCR, western blotting, and immunofluorescence (IF) in cell lines. The effects of exogenous expression of JAM3 using lentiviral vectors on invasion, adhesion, and apoptosis were verified using transwell assays and flow cytometry. Differentially expressed genes (DEGs) were detected by RNA sequencing and verified by q‒PCR and Western blotting. The effect of JAM3 silencing using siRNA was assessed by an adhesion assay. Kaplan‒Meier analysis was applied to calculate the impact of JAM3 expression and classic clinicopathologic characteristics on survival. Results: Bioinformatics analysis revealed that JAM3 expression was reduced in BCBM. Exogenous expression of JAM3 minimizes the ability of breast cancer cells to invade and adhere and promotes their apoptosis. Silencing JAM3 results in morphology changes and the recovery of invasion and adhesion to ECMs, and the TGF-β/Smad signaling pathway may be involved. JAM3 predicts less metastasis and good survival in patients with BCBM. Statistical analysis of BCBM samples detected by immunohistochemistry (IHC) and the associated clinicopathological characteristics revealed that low levels of JAM3 expression and high levels of TNF-β1 are linked to the clinical progression of both primary and metastatic breast tumors. Kaplan–Meier analysis revealed that a high expression level of JAM3 was associated with longer survival. Conclusion: JAM3 can serve as a key negative regulator of breast cancer cell invasion, apoptosis, and brain metastasis, possibly through the TGF/Smad signaling pathway. JAM3 is anticipated to be a promising biomarker for the diagnosis and prognosis of breast cancer. [ABSTRACT FROM AUTHOR]

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]

The study aimed to utilize network pharmacology combined with cell experiments to research the mechanism of action of Saikosaponin-d in the treatment of gastric cancer. Drug target genes were obtained from the PubChem database and the Swiss Target Prediction database. Additionally, target genes for gastric cancer were obtained from the GEO database and the Gene Cards database. The core targets were then identified and further analyzed through gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and GESA enrichment. The clinical relevance of the core targets was assessed using the GEPIA and HPA databases. Molecular docking of drug monomers and core target proteins was performed using Auto Duck Tools and Pymol software. Finally, in vitro cellular experiments including cell viability, apoptosis, cell scratch, transwell invasion, transwell migration, qRT-PCR, and Western blot were conducted to verify these findings of network pharmacology. The network pharmacology analysis predicted that the drug monomers interacted with 54 disease targets. Based on clinical relevance analysis, six core targets were selected: VEGFA, IL2, CASP3, BCL2L1, MMP2, and MMP1. Molecular docking results showed binding activity between the Saikosaponin-d monomer and these core targets. Saikosaponin-d could inhibit gastric cancer cell proliferation, induce apoptosis, and inhibit cell migration and invasion. [ABSTRACT FROM AUTHOR]

Copyright of Acta Scientiarum Naturalium Universitatis Sunyatseni / Zhongshan Daxue Xuebao is the property of Sun-Yat-Sen University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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Background: Triple‐negative breast cancer, a subtype of breast cancer, is characterized by a poor prognosis. Recent studies have shown that miRNA30b acts as an oncogene and is vital for the proliferation of malignancies across various systems. This study aimed to elucidate the impact of miRNA30b on the proliferation, migration, and invasion capabilities of breast cancer cells in vitro. Methods: Triple‐negative breast cancer cell lines MDA‐MB‐231 were transiently transfected with miRNA30b inhibitor, mimic, or the negative control by Lipofectamine 2000. Successful transfection was confirmed by quantitative real‐time polymerase chain reaction (qRT‐PCR). Functional assays, including CCK8, clone formation, scratch, and transwell assays, were conducted to evaluate the proliferation, invasion, and migration ability of MDA‐MB‐231 cells in each group. The target protein of miRNA30b was determined using an online prediction data website, and the dual‐luciferase assay confirmed whether there was a binding site between miRNA30b and ADAM12. The effect was further verified by Western blot analysis. Results: MDA‐MB‐231 cells were transfected with miRNA30b inhibitor, mimic, and negative control. miRNA30b expression was downregulated in the cells. Relative to the negative control group, miRNA30b expression significantly increased in the mimic group and decreased in the miRNA30b inhibitor group, with the differences being statistically significant. The miRNA30b mimic group exhibited a significant increase in miRNA30b expression and a corresponding promotion of cell proliferation, colony formation, and migration. Conversely, the miRNA30b inhibitor group displayed significantly reduced miRNA30b expression and suppressed cell proliferation, colony formation, and migration abilities compared to the negative control cells. Bioinformatics software predicted ADAM12 as a potential target of miRNA30b. Dual‐luciferase assays confirmed the presence of a binding site between miRNA30b and ADAM12. Western blot analysis revealed that overexpression of miRNA30b downregulated ADAM12 expression in MDA‐MB‐231 cells. Conclusions: miRNA30b could promote proliferation, migration, and invasion of TNBC cell lines MDA‐MB‐231. The effect of miRNA30b on triple‐negative breast cancer would be achieved partly at least through inhibiting the expression of ADAM12. [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]

AIM: To investigate the impact of platycodin D （PD） on the viability, migration, invasion, apoptosis and cell cycle of osteosarcoma cells in vitro, along with its underlying mechanisms. METHODS: Human osteosarcoma cells MG63 and U2OS were divided into control group （0 μmol/L） and PD treatment group （6. 25, 12. 5, 25, 50 and 100 μmol/L, respectively）. Human osteosarcoma cells MG63 and U2OS were categorized into control groups （0 μmol/L PD） and PD treatment groups （6. 25, 12. 5, 25, 50 and 100 μmol/L）. The CCK-8 assay determined cell viability and identified effective treatment concentrations. MG63 （15 μmol/L PD） and U2OS （25 μmol/L PD） were specifically analyzed. Cell scratch and Transwell assays assessed migration and invasion. Hoechst 33342 staining examined nuclear morphological changes. Flow cytometry analyzed cell cycle distribution and apoptosis rate. Western blot measured protein expression levels: cleaved caspase-3, cleaved PARP, c-Jun N-terminal kinase （JNK）, p-JNK, B-cell lymphoma-2 （Bcl2）, Bcl-2-ssociated X protein （BAX）, matrix metalloproteinase 2 （MMP-2）, MMP-9, cyclin-dependent kinase 4 （CDK4）, cyclin D1, CDK1, cyclin B1, extracellular signal-regulated kinase （ERK） and p-ERK. Proteome sequencing of MG63 cells was performed. RESULTS: PD treatment significantly decreased cell survival, scratch healing rate, and invasive cell numbers, while increasing apoptosis rates （P<0. 05）. Morphological changes such as nuclear hyperchromatism and fragmentation were observed in PD-treated cells. PD induced G2/M phase arrest in MG63 and G0/G1 phase arrest in U2OS cells. PD treatment upregulated BAX, cleaved caspase-3, cleaved PARP, and p-JNK/JNK, while downregulating Bcl-2, MMP-2, MMP-9, CDK4, cyclin D1, CDK1, cyclin B1, and p-ERK/ERK（ P<0. 05）. Proteome sequencing revealed PD's involvement in cell division, cell cycle regulation, focal adhesion, apoptosis, and the MAPK signaling pathway. CONCLUSION: PD inhibits cell viability, migration, and invasion of osteosarcoma cells in vitro, while promoting apoptosis and inducing cell cycle arrest. These effects are likely mediated through modulation of the MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Purpose: Preeclampsia (PE) is a pregnancy-specific syndrome with increasing maternal and perinatal morbidity and mortality. Succinylation, a post-translational modification event, has been found in various diseases. However, the role of succinylation in PE has not been explored. This study aimed to investigate the effect of succinylation on PE and the underlying mechanisms. Methods: Thirty-two PE patients and 32 normal pregnancy volunteers were recruited. Human extravasated trophoblast cells (HTR-8/SVneo) were used in in vitro study. RT-qPCR was performed to detect the expression of succinylation-related mRNAs. The cell proliferation, invasion, and migration were assessed using cell counting kit-8, ethynyldeoxyuridine, transwell, and wound healing assays. Co-immunoprecipitation and dual-luciferase reporter assays were performed to analyze the interaction between sirtuin (SIRT)5 and homeobox box 3 (HOXB3). Results: SIRT5 was increased in the placental tissues of PE patients. SIRT5 inhibition increased cell proliferation, invasion, and migration in HTR-8/SVneo cells. Mechanistic investigations indicated that HOXB3 was a downstream regulatory target of SIRT5-mediated desuccinylation. Rescue experiments further verified that silencing of HOXB3 inhibited cell proliferation, invasion, and migration. Additionally, HOXB3 deficiency reversed the activation of the Notch and β-catenin signaling pathway induced by SIRT5 inhibition. Conclusion: SIRT5 inhibited the trophoblast cell proliferation, invasion, and migration to promote PE through suppressing Notch and β-catenin signaling pathway activation via desuccinylating HOXB3. [ABSTRACT FROM AUTHOR]

Introduced species may exhibit variations in their preferred climatic niches between their native and introduced ranges, which can have important implications for the transferability of distribution models. In the Himalayan ecoregion, little is known about the geographic distribution and climatic niche overlap between native and introduced cold‐water species. Here, we used the COUE (centroid shift, overlap, unfilling, and expansion) framework to explore the invasive potential of rainbow (Oncorhynchus mykiss) and brown (Salmo trutta fario) trout and corresponding climatic niche overlap with native snow trout (Schizothorax plagiostomus and Schizothorax richardsonii) in the Indus and Ganges River basins. Although we found more stability in the climatic niche for O. mykiss (93%) than S. trutta (58%), both species do not conserve their climatic niches in this region (p > 0.05). S. trutta has expanded more toward new environmental conditions (42%) compared to O. mykiss (7%). However, there are still available environmental gaps that O. mykiss and S. trutta can potentially occupy in the future. There was a higher overlap in climatic niches between S. plagiostomus and O. mykiss and between S. richardsonii and S. trutta. Observed shifts in climatic niches of these introduced species can negatively affect the transferability of distribution models, which may underestimate the assessments of habitat suitability for introduced trout in the Himalayas. Our study demonstrates that the information on climatic niche dynamics can inform the model‐building process and improve the transferability and predictive performance to better assess vulnerability of sensitive habitats to introduced species in the Himalayas and elsewhere. [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]