Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-05-05DOI: 10.1080/19336918.2026.2663684
Yu-Ling A Kao, Qiaochu Wang, Dajun D Lu, Shigeki Umemura, Vivien Lee, Ying Hsuan Tsai, Robert B Barndt, Jehng-Kang Wang, Michael D Johnson, Chen-Yong Lin
{"title":"Dynamic modulation of intercellular adhesion mediated by matriptase-EPCAM/Trop-2 axes is critical for cell extrusion, division, and collective migration.","authors":"Yu-Ling A Kao, Qiaochu Wang, Dajun D Lu, Shigeki Umemura, Vivien Lee, Ying Hsuan Tsai, Robert B Barndt, Jehng-Kang Wang, Michael D Johnson, Chen-Yong Lin","doi":"10.1080/19336918.2026.2663684","DOIUrl":"10.1080/19336918.2026.2663684","url":null,"abstract":"<p><p>Epithelial dynamics require rapid remodeling of cell adhesion during extrusion, division, and migration. We identify a matriptase-dependent mechanism regulating the Ca<sup>2+</sup>- independent adhesion molecules EpCAM and Trop-2. Matriptase activation cleaves these CAMs into two-chain forms, promoting internalization and degradation, followed by replenishment through new synthesis. This turnover enables rapid adaptation of adhesion to environmental cues. Loss of matriptase disrupts this cycle, impairing epithelial integrity, extrusion, mitosis, and collective migration. Matriptase activity is tightly controlled by zymogen activation and inhibition by HAI-1, restricting CAM cleavage. Environmental factors, including pH, redox state, and chloride levels, modulate activation, linking external stimuli to adhesion remodeling. This protease-driven pathway provides a rapid, adaptable system for epithelial adhesion control.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2663684"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-01-31DOI: 10.1080/19336918.2026.2620945
Hailong Li, Dong Wei, Xiaqing Gao, Rong Su, Chunting Yang, Ping Tang, Xiqiu Yu, Yuhong Wu
{"title":"COPB2 drives gastric cancer progression via PI3K/AKT/NF-κB signaling: a multi-omics and functional study.","authors":"Hailong Li, Dong Wei, Xiaqing Gao, Rong Su, Chunting Yang, Ping Tang, Xiqiu Yu, Yuhong Wu","doi":"10.1080/19336918.2026.2620945","DOIUrl":"10.1080/19336918.2026.2620945","url":null,"abstract":"<p><p>This study investigated the role of COPB2 in gastric cancer (GC) pathogenesis. Analysis of TCGA datasets and tissue microarrays revealed its upregulation in GC tissues compared to normal adjacent tissues, which was correlated with advanced tumor stage and lymphatic invasion and demonstrated significant diagnostic value (AUC = 0.895 and 0.851). Functional assays using lentiviral-mediated silencing in GC cells showed that COPB2 knockdown suppressed cell proliferation and migration, induced G0/G1-phase arrest, and promoted apoptosis. Mechanistic investigations through microarray, KEGG, and IPA analyses indicated that COPB2 dysregulation inactivated the PI3K/AKT and NF-κB signaling pathways. This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2620945"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"EPB41L family serves as a prognostic biomarker for kidney renal clear cell carcinoma.","authors":"Gonglin Tang, Kai Sun, Guixin Ding, Jitao Wu, Jian Ma, Hongwei Zhao","doi":"10.1080/19336918.2026.2624964","DOIUrl":"10.1080/19336918.2026.2624964","url":null,"abstract":"<p><p>EPB41L1-5 is known to maintain cell morphology and signal transduction, with evidence suggesting it can inhibit tumor progression. However, its role in kidney renal clear cell carcinoma (KIRC) is not fully understood. This study evaluated EPB41L1-5's prognostic value in KIRC using bioinformatics methods and validation through qPCR, immunohistochemistry, and cell functional experiments. The results demonstrated a decreased expression of EPB41L in KIRC tissue compared to normal renal tissue, correlating with lower survival rates. Low EPB41L expression was also associated with overall survival in KIRC. Additionally, EPB41L was found to be involved in extracellular matrix regulation, G protein-coupled receptor ligand binding, and multiple immune cell infiltrations. In addition, their elevated methylation levels are associated with poor prognosis in KIRC patients. Overall, EPB41L family is a potential molecular marker for predicting KIRC prognosis, offering insights for therapeutic development.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2624964"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12885433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-04-01DOI: 10.1080/19336918.2026.2650871
Natalia Świsłocka, Anna Pryczynicz, Justyna Dorf, Konrad Zaręba, Katarzyna Guzińska-Ustymowicz
{"title":"TNS1 and TNS4 play a potential role in development of pancreatic ductal adenocarcinoma but not TNS2 and TNS3.","authors":"Natalia Świsłocka, Anna Pryczynicz, Justyna Dorf, Konrad Zaręba, Katarzyna Guzińska-Ustymowicz","doi":"10.1080/19336918.2026.2650871","DOIUrl":"10.1080/19336918.2026.2650871","url":null,"abstract":"<p><p>Tensins are a family of adhesion proteins that play a role in constructing the cytoskeleton, as well as in intracellular and extracellular communication. Their expression was evaluated in 22 pancreatic cancer patients using the immunohistochemistry method. TNS1 expression occurred more frequently among patients with tumor diameter ≥ 2 cm, which may suggest an association with the development of pancreatic cancer. Intraductal TNS1 was observed less often with presence of necrosis and hemorrhages in tumor. The fact that cancer cells secrete TNS1 suggests that it could be investigated as a potential target for liquid biopsies. TNS4 expression occurred more frequently among females and was observed when necrosis in tumor was strong. TNS2 and TNS3 are not involved in the development of ductal pancreatic adenocarcinoma.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2650871"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-09-06DOI: 10.1080/19336918.2026.2728214
Qing Hu, Renfan Zhang, Yefeng Zhou, Yang Yang, Hao Zhou, Xin Han, Shengrong Lin
{"title":"GJB2, a novel transcription target of HSF4, confers tumorigenic and metastatic phenotypes and sustains mitochondrial homeostasis in lung adenocarcinoma via the PI3K/AKT pathway.","authors":"Qing Hu, Renfan Zhang, Yefeng Zhou, Yang Yang, Hao Zhou, Xin Han, Shengrong Lin","doi":"10.1080/19336918.2026.2728214","DOIUrl":"https://doi.org/10.1080/19336918.2026.2728214","url":null,"abstract":"<p><p>The ion channel gene GJB2 emerges as a therapeutic target for LUAD with significant prognostic value. Herein, the potential mechanisms of GJB2 were investigated. GJB2 expression was analyzed by bioinformatics, RT-qPCR and western blotting. In vitro functional assays and A549 xenografts detected the role of GJB2. The upstream mechanism of GJB2 was explored. GJB2 was up-regulated and associated with the poor overall survival of LUAD patients. GJB2 knockdown inhibited cell malignancy and impaired mitochondrial homeostasis. HSF4 enhanced GJB2 transcription. GJB2 knockdown lowered PI3K/AKT activity. SC79 reversed the in vitro impacts of GJB2 inadequacy and promoted tumor growth when HSF4 was up-regulated and GJB2 was down-regulated simultaneously. GJB2, transcriptionally activated by HSF4, activates PI3K/AKT pathway to support LUAD tumorigenesis and development.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2728214"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"POU2F2 as a dual oncogenic and immunomodulatory driver in kidney renal clear cell carcinoma.","authors":"Gonglin Tang, Fei Liu, Mingze Sun, Chenyue Liu, Jitao Wu, Hongwei Zhao","doi":"10.1080/19336918.2026.2700062","DOIUrl":"10.1080/19336918.2026.2700062","url":null,"abstract":"<p><p>Kidney renal clear cell carcinoma (KIRC) features an immunosuppressive tumor microenvironment (TME). We investigated the role of transcription factor POU2F2 in KIRC oncogenesis and macrophage polarization. Single-cell and spatial transcriptomics showed that POU2F2 is upregulated in KIRC and associated with metastasis and poor prognosis. POU2F2 knockdown inhibited KIRC cell proliferation, migration, and invasion in vitro. POU2F2 expression correlated with macrophage infiltration and JAK-STAT signaling. Co-culture assays showed that POU2F2 silencing reduced macrophage recruitment and shifted M2 polarization toward an anti-tumor M1 phenotype. Overall, POU2F2 acts as an oncogenic driver and prognostic biomarker in KIRC, promoting an immunosuppressive TME and representing a potential therapeutic target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2700062"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13353782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-01-27DOI: 10.1080/19336918.2026.2616948
Jie Sun, Yaqian Liu, Jieji Mo, Jialin Zhou, Xue Bai, Boshi Gu, Jun Li, Haidong Zhao
{"title":"NCEH1 promotes breast cancer progression by regulating NRP1 and activating the TNF-α/NF-κB signalling pathway.","authors":"Jie Sun, Yaqian Liu, Jieji Mo, Jialin Zhou, Xue Bai, Boshi Gu, Jun Li, Haidong Zhao","doi":"10.1080/19336918.2026.2616948","DOIUrl":"10.1080/19336918.2026.2616948","url":null,"abstract":"<p><strong>Purpose: </strong>Neutral cholesterol ester hydrolase 1 (NCEH1), a key enzyme in cellular lipid metabolism, is associated with cancer progression. Its molecular functions in breast cancer remain poorly understood.</p><p><strong>Methods: </strong>This study evaluated the expression of NCEH1 in breast cancer patients using multiple databases. Functionally, the effects of NCEH1 silencing or overexpression on breast cancer cell growth and motility were investigated. RNA-seq was employed to identify downstream target genes and signalling pathways.</p><p><strong>Results: </strong>The expression of NCEH1 in breast cancer tissues and cells was significantly higher than that in normal tissues and cells. Silencing NCEH1 suppressed breast cancer cell proliferation and migration. Mechanistically, NCEH1 regulated Neuropilin-1 (NRP1) expression, and both promoted malignant phenotypes in breast cancer by activating the TNF-α/NF-κB signalling pathway.</p><p><strong>Conclusion: </strong>Our findings demonstrate that NCEH1 accelerates breast cancer progression by modulating NRP1 and activating the TNF-α/NF-κB signalling pathway. Collectively, NCEH1 represents a potential novel biomarker and therapeutic target for breast cancer.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2616948"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12851389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2026-12-01Epub Date: 2026-04-19DOI: 10.1080/19336918.2026.2658289
Jie Ruan, Ying Xie, Chaoqun Zhang, Dianxing Sun
{"title":"Meox1 promotes hepatocellular carcinoma progression potentially via regulation of cell cycle and p21 expression.","authors":"Jie Ruan, Ying Xie, Chaoqun Zhang, Dianxing Sun","doi":"10.1080/19336918.2026.2658289","DOIUrl":"10.1080/19336918.2026.2658289","url":null,"abstract":"<p><p>Meox1 is aberrantly expressed in several malignancies, but its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate the effects of Meox1 on HCC cells and explore the underlying molecular mechanisms. Cell proliferation, colony formation, migration, invasion, and cell cycle distribution were assessed by CCK-8, clonogenic, Transwell, and flow cytometry assays, respectively. Protein expression was examined by Western blotting. Meox1 silencing significantly inhibited proliferation, clonogenic capacity, migration and invasion of HCC cells. Cell cycle analysis showed a reduction in G1-phase cells with a marked accumulation in the G2 phase following Meox1 knockdown. Western blot analysis revealed that suppression of Meox1 reduced p21CIP1/WAF1 expression. Meox1 contributest to HCC progression and may represent a potential therapeutic target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2658289"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2025-12-01Epub Date: 2025-06-03DOI: 10.1080/19336918.2025.2514374
Uri Han, Nara Han, Taeck Joong Jeon
{"title":"Nhe1 is required for directional sensing in vegetative <i>Dictyostelium</i> cell migration.","authors":"Uri Han, Nara Han, Taeck Joong Jeon","doi":"10.1080/19336918.2025.2514374","DOIUrl":"10.1080/19336918.2025.2514374","url":null,"abstract":"<p><p>Na+/H+ exchanger 1 (Nhe1) is a crucial regulator of pH homeostasis and the present study demonstrates that Nhe1 is required for directional sensing in vegetative <i>Dictyostelium</i> cell migration. <i>nhe1</i> null cells exhibited severe defects in directional sensing and migration in response to folate gradients and applied electric fields.Specifically, <i>nhe1</i> null cells failed to exhibit proper translocation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) to the cell cortex and showed abnormal intracellular calcium signaling upon folate stimulation. Additionally, cells lacking Nhe1 exhibited a reduced capacity to engulf bacteria and latex beads. In contrast, <i>nhe1</i> null cells in the developed stage displayed a defect in cAMP-directed chemotaxis, but normal translocation kinetics of PIP3 to the cell cortex upon cAMP stimulation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2514374"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"N-Acetylcysteine relieving hydrogen peroxide-induced damage in granulosa cells of sheep.","authors":"Hao Chen, Jine Wang, Bingzhu Zhao, Yahua Yang, Chongfa Yang, Zhijie Zhao, Xiaona Ding, Yang Li, Taojie Zhang, Zhaxi Yingpai, Shengdong Huo","doi":"10.1080/19336918.2025.2484182","DOIUrl":"10.1080/19336918.2025.2484182","url":null,"abstract":"<p><p>Sheep ovarian granulosa cells (GCs) play a unique role in the ovary. Damage to GCs can affect the normal development of oocytes. The oxidative stress model was constructed by H<sub>2</sub>O<sub>2</sub>to study the biological changes. Specifically, pathological characteristic was assessed by immunohistochemistry (IHC), while signaling pathway was studied using western blot, quantitative RT-PCR, and immunofluorescence. Theresults showed that the oxidative damage model was successfully constructed by 200 μmol/LH<sub>2</sub>O<sub>2</sub> for 12 h. NAC can protect the proliferation of GCs under H<sub>2</sub>O<sub>2</sub>-induced oxidative stress and reduce apoptosis. It can also promote the secretion of E<sub>2</sub> and P<sub>4</sub> by GCs and reduce the inflammatory response of GCs. NAC can enhance the expression of NRF2, PI3K and Akt. These findings suggest that NAC alleviates H<sub>2</sub>O<sub>2</sub>-induced oxidative stress injury through NRF2/PI3K/AKT signaling pathways. Provide ideas for studying the poor quality of mammalian oocytes.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2484182"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}