Cell Adhesion & Migration最新文献

Abnormal expression of galectins and their correlation with fibrogenesis in adenomyosis. 血凝素在子宫腺肌症组织中的异常表达及其与纤维形成的关系。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-31 Epub Date: 2026-05-20 DOI: 10.1080/19336918.2026.2658283

Yuan Zhou, Mengdong Cao, Zhenzhen Wang, Yaonan Yu, Han Yu, Xue Shen

引用次数: 0

STED/AFM as a tool to investigate mechanical and adhesive properties of migrating keratinocytes. STED/AFM作为研究迁移角化细胞力学和粘附特性的工具。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-31 Epub Date: 2026-04-15 DOI: 10.1080/19336918.2026.2657675

Mariya Y Radeva, Jens Waschke, Michael Fuchs

引用次数: 0

G protein-coupled estrogen receptor (GPER) modulates epithelial-mesenchymal transition-like phenotype in human glioblastoma cells. G蛋白偶联雌激素受体（GPER）调节人胶质母细胞瘤细胞上皮-间充质过渡样表型。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-31 Epub Date: 2026-08-21 DOI: 10.1080/19336918.2026.2720325

Karla Mariana Peña-Gutiérrez, Karina Hernández-Ortega, Beatriz Arantxa Castro-Reyes, Andrea Rosas-Benitez, Edgar Ricardo Vázquez-Martínez, Rocío García-Becerra, Ignacio Camacho-Arroyo

{"title":"G protein-coupled estrogen receptor (GPER) modulates epithelial-mesenchymal transition-like phenotype in human glioblastoma cells.","authors":"Karla Mariana Peña-Gutiérrez, Karina Hernández-Ortega, Beatriz Arantxa Castro-Reyes, Andrea Rosas-Benitez, Edgar Ricardo Vázquez-Martínez, Rocío García-Becerra, Ignacio Camacho-Arroyo","doi":"10.1080/19336918.2026.2720325","DOIUrl":"10.1080/19336918.2026.2720325","url":null,"abstract":"Glioblastomas (GBs) are the most frequent and aggressive central nervous system tumors, whose progression is influenced by sex hormones. 17β-estradiol (E2), promotes an epithelial-to-mesenchymal transition (EMT)-like process and enhances proliferative, migratory, and invasive capacities in GB through intracellular estrogen receptors. However, the role of G protein-coupled estrogen receptor (GPER) in GB remains poorly understood. We evaluated the effects of E2, the GPER-agonist G-1, and the GPER-antagonist G-15 on EMT-related processes, migration, and invasion in U251 and U87 GB-derived cells. GPER activation by E2 and G-1 increased migration and invasion, whereas G-15, alone or combined, reduced these effects. GPER activation also induced a mesenchymal-like phenotype. These findings suggest that GPER-associated signaling contributes to EMT-like phenotypic changes, migration, and invasion in GB.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2720325"},"PeriodicalIF":4.3,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13502043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788605","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}

引用次数: 0

LncRNA UNC5C-AS1 inhibits angiogenesis and induces endothelial apoptosis via the miR-148a-3p/EMP1 axis in preeclampsia. LncRNA UNC5C-AS1在子痫前期通过miR-148a-3p/EMP1轴抑制血管生成并诱导内皮细胞凋亡。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-02-06 DOI: 10.1080/19336918.2026.2622820

Yang Wang, Yan Gao, Lingfang Liu, Ke Ma, Yingying He, Hongbo Qi, Xuemei Zhang

引用次数: 0

Research on tissue-resident macrophages in the field of cancer research: a bibliometric analysis from 2004 to 2025. 组织驻留巨噬细胞在癌症研究领域的研究：2004年至2025年的文献计量分析。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-02-02 DOI: 10.1080/19336918.2026.2624204

Qingya Song, Zongliang Yu, Wenping Lu, Qingyuan Chi

引用次数: 0

CXCL11 secreted by cancer-associated fibroblasts promotes nasopharyngeal carcinoma progression via CXCR3/PD-L1 axis. 癌症相关成纤维细胞分泌的CXCL11通过CXCR3/PD-L1轴促进鼻咽癌进展。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-05-04 DOI: 10.1080/19336918.2026.2665498

Jie Fang, Huijuan Cheng, Peng Zhang, Liang Wang

{"title":"CXCL11 secreted by cancer-associated fibroblasts promotes nasopharyngeal carcinoma progression via CXCR3/PD-L1 axis.","authors":"Jie Fang, Huijuan Cheng, Peng Zhang, Liang Wang","doi":"10.1080/19336918.2026.2665498","DOIUrl":"10.1080/19336918.2026.2665498","url":null,"abstract":"The secretion of chemokines by cancer-associated fibroblasts (CAFs) is a critical driver of cancer progression. Nevertheless, the precise contribution of CAFs in the nasopharyngeal carcinoma (NPC) tumor microenvironment to disease progression is yet to be fully understood. In this study, C-X-C motif chemokine ligand 11 (CXCL11) was identified to be upregulated in tumor tissues of NPC patients and NPC cells compared to counterpart normal tissues and cell lines. The CAFs-secreted CXCL11 was found to enhance the proliferative, invasive, and migratory capacities of NPC cells. CAFs-derived CXCL11 upregulates CXCR3 expression to facilitate NPC cell proliferation, migration, and invasion. Through mechanism investigation, we confirmed that CXCL11/CXCR3 axis upregulated PD-L1 expression through p65-mediated transcription activation. Finally, in vivo experiments further validated the tumor-promoting role of CAFs-secreted CXCL11 in NPC. In conclusion, our findings reveal a novel mechanism wherein CAFs-secreted CXCL11 promotes NPC malignant progression by activating the CXCR3/PD-L1 signaling axis.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2665498"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13155017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811603","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}

引用次数: 0

N6-methyladenosine modification of NEU1 mediated by METTL3 exacerbates angiotensin II-induced atrial fibrillation. METTL3介导的NEU1的n6 -甲基腺苷修饰加重了血管紧张素ii诱导的心房颤动。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-03-31 DOI: 10.1080/19336918.2026.2650272

Zhilan Zhang, Yanbing Luo, Qiuguo Zou, Zelai Mo

引用次数: 0

RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression. rbm15b介导的m6A修饰FOXM1激活AURKA/TPX2轴，促进上皮-间质过渡驱动的子宫内膜癌进展。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-05-18 DOI: 10.1080/19336918.2026.2674357

Lijing Zhang, Ping Wu

{"title":"RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression.","authors":"Lijing Zhang, Ping Wu","doi":"10.1080/19336918.2026.2674357","DOIUrl":"10.1080/19336918.2026.2674357","url":null,"abstract":"Endometrial cancer(EC) is increasing worldwide, but its molecular mechanisms remain unclear. This study explored whether RBM15B-mediated m6A modification of FOXM1 promotes EC progression through the AURKA/TPX2 axis and epithelial-mesenchymal transition(EMT). Bioinformatics analyses assessed FOXM1 expression and prognosis in EC. RNA pull-down, MeRIP-PCR, dot blot, and RNA stability assays examined m6A regulation. Colony formation, Transwell, wound healing, and tumor sphere assays evaluated malignant behaviors. FOXM1 was significantly upregulated in EC and associated with unfavorable prognosis. Functional assays showed that FOXM1 enhanced proliferation, migration, invasion, and stemness of EC cells. Mechanistically, RBM15B increased m6A modification of FOXM1 mRNA and promoted expression. RBM15B knockdown inhibited malignant phenotypes and reduced activation of the downstream AURKA/TPX2 pathway. RBM15B-mediated m6A methylation stabilizes FOXM1 expression, activates the AURKA/TPX2 axis, and promotes EMT and EC progression. Targeting the RBM15B/FOXM1/AURKA/TPX2 pathway may offer therapeutic potential.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2674357"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13185462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147962362","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}

引用次数: 0

Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway. LTF的上调通过激活PI3K/AKT通路促进左侧结直肠癌的发展。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-01-09 DOI: 10.1080/19336918.2026.2613628

Peng Chen, Mingrui Zhang, Xuefeng Bai

{"title":"Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway.","authors":"Peng Chen, Mingrui Zhang, Xuefeng Bai","doi":"10.1080/19336918.2026.2613628","DOIUrl":"10.1080/19336918.2026.2613628","url":null,"abstract":"Lactoferrin (LTF) has gained attention as a potential anti-cancer biomarker, but its role in left-sided colon cancer (LCC) remains poorly understood. This study explores the function of LTF in LCC and its underlying mechanisms. LTF expression was significantly elevated in tumor tissues compared to normal tissues (59.67-fold increase, p < .001). LTF overexpression significantly enhanced LCC cell proliferation, migration, and invasion (p < .01), while suppressing apoptosis (p < .05). In contrast, LTF knockdown markedly inhibited these oncogenic behaviors. Western blot analysis demonstrated that LTF overexpression led to increased phosphorylation of PI3K and Akt proteins (p < .01), suggesting activation of the PI3K/AKT signaling pathway, while LTF knockdown resulted in decreased phosphorylation levels (p < .01). This study identifies LTF as a promoter of LCC development via activation of the PI3K/AKT pathway, suggesting LTF as a promising therapeutic target. Further research is warranted to evaluate its clinical potential in LCC treatment.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2613628"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942266","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}

引用次数: 0

NAT10 promotes proliferation, invasion, and epithelial-mesenchymal transition in hepatocellular carcinoma through α-tubulin acetylation. NAT10通过α-微管蛋白乙酰化促进肝癌细胞的增殖、侵袭和上皮-间质转化。

IF 4.3 3区生物学

Cell Adhesion & Migration Pub Date : 2026-12-01 Epub Date: 2026-08-24 DOI: 10.1080/19336918.2026.2697609

Haogang Yu, Kankai Zhu, Guoliang Zhang, Yang Dong, Xiaodong Wang, Shufen Zhang, Jiajing Huang, Xuemei Lu, Xiuming Zhang, Hao Liu, Wei Chen

{"title":"NAT10 promotes proliferation, invasion, and epithelial-mesenchymal transition in hepatocellular carcinoma through α-tubulin acetylation.","authors":"Haogang Yu, Kankai Zhu, Guoliang Zhang, Yang Dong, Xiaodong Wang, Shufen Zhang, Jiajing Huang, Xuemei Lu, Xiuming Zhang, Hao Liu, Wei Chen","doi":"10.1080/19336918.2026.2697609","DOIUrl":"10.1080/19336918.2026.2697609","url":null,"abstract":"Hepatocellular carcinoma (HCC) remains a global health challenge due to its high metastatic potential and poor prognosis. This study investigated the role and underlying molecular mechanisms of N-acetyltransferase 10 (NAT10)-mediated α-tubulin acetylation in HCC progression. Using Huh-7 and SNU-449 cell lines, we established stable knockdown and overexpression models to systematically evaluate both gain- and loss-of-function effects. Functional assays revealed that NAT10 suppression significantly decreased α-tubulin acetylation, thereby inhibiting cell proliferation, invasion, and migration. Conversely, NAT10 overexpression promoted these oncogenic traits. In vivo validation confirmed NAT10 accelerates tumor growth and lung metastasis. Treatment with the NAT10 inhibitor Remodelin partially reversed the phenotypic effects of NAT10 overexpression and restored epithelial - mesenchymal transition (EMT) marker expression. In conclusion, our results demonstrate that NAT10 drives HCC progression by regulating the α-tubulin acetylation axis, highlighting its potential as a promising therapeutic target for combating HCC metastasis.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2697609"},"PeriodicalIF":4.3,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812022","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}

引用次数: 0