Cell Adhesion & Migration最新文献

{"title":"Activation of GRP78 ATPase suppresses A549 lung cancer cell migration by promoting ITGB4 degradation.","authors":"Junya Ning,&nbsp;Xiaoling Cui,&nbsp;Nan Li,&nbsp;Na Li,&nbsp;Baoxiang Zhao,&nbsp;Junying Miao,&nbsp;Zhaomin Lin","doi":"10.1080/19336918.2022.2130415","DOIUrl":"https://doi.org/10.1080/19336918.2022.2130415","url":null,"abstract":"<p><p>Hypochlorous acid (HOCl) is an essential signal molecule in cancer cells. Activated GRP78 ATPase by a HOCl probe named ZBM-H inhibits lung cancer cell growth. However, the role and underlying mechanism of GRP78 ATPase in lung cancer cell migration have not been established. Here, we reported that activation of GRP78 ATPase by ZBM-H suppressed A549 cell migration and inhibited EMT process. Notably, ZBM-H time-dependently decreased the protein level of integrin β4 (ITGB4) in A549 cells. Combinatorial treatment of 3BDO (an autophagy inhibitor) and ZBM-H partially rescued the protein level of ITGB4. Consistently, 3BDO partially reversed ZBM-H-inhibited cell migration. Furthermore, ZBM-H promoted the interaction between ANXA7 and Hsc70, which participated in the regulation of selective autophagy and degradation of ITGB4.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9542429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10637614","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":"TNF-α regulates the composition of the basal lamina and cell-matrix adhesions in gingival epithelial cells.","authors":"Masaru Mezawa,&nbsp;Yuto Tsuruya,&nbsp;Arisa Yamaguchi,&nbsp;Mizuho Yamazaki-Takai,&nbsp;Tetsuro Kono,&nbsp;Hiroyuki Okada,&nbsp;Christopher A McCulloch,&nbsp;Yorimasa Ogata","doi":"10.1080/19336918.2022.2029237","DOIUrl":"https://doi.org/10.1080/19336918.2022.2029237","url":null,"abstract":"<p><p>Laminin 5, type 4 collagen, and α6β4 integrin contribute to the formation of hemidesmosomes in the epithelia of periodontal tissues, which is critical for the development and maintenance of the dentogingival junction. As it is not known whether TNF-α alters the composition of the epithelial pericellular matrix, human gingival epithelial cells were cultured in the presence or absence of TNF-α. Treatment with TNF-α accelerated epithelial cell migration and closure of in vitro wounds. These data indicate unexpectedly, that TNF-α promotes the formation of the pericellular matrix around epithelial cells and enhances adhesion of epithelial cells to the underlying matrix, properties which are important for cell migration and the integrity of the dentogingival junction.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39764444","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":"Novel role of Dipterocarpus tuberculatus as a stimulator of focal cell adhesion through the regulation of MLC2/FAK/Akt signaling pathway","authors":"Su jin Lee, Ji Eun Kim, J. W. Jung, Y. Choi, J. Gong, Bounleuane Douangdeuane, Onevilay Souliya, Y. Choi, Sung Baek Seo, D. Hwang","doi":"10.1080/19336918.2022.2073002","DOIUrl":"https://doi.org/10.1080/19336918.2022.2073002","url":null,"abstract":"ABSTRACT To investigate a novel function of Dipterocarpus tuberculatus on focal cell adhesion stimulation, alterations to the regulation of focal cell adhesion-related factors were analyzed in NHDF cells and a calvarial defect rat model after treatment with methanol extracts of D. tuberculatus (MED). MED contained gallic acid, caffeic acid, ellagic acid, and naringenin in high concentrations. The proliferation activity, focal cell adhesion ability, adhesion receptors-mediated signaling pathway in NHDF cells were increased by MED. Also, a dense adhered tissue layer and adherent cells on MED-coated titanium plate (MEDTiP) surfaces were detected during regeneration of calvarial bone. The results of the present study provide novel evidence that MED may stimulate focal cell adhesion in NHDF cells and a calvarial defect rat model.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46930438","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":"Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway","authors":"E. Dukhanina, T. Portseva, A. Dukhanin, S. Georgieva","doi":"10.1080/19336918.2022.2072554","DOIUrl":"https://doi.org/10.1080/19336918.2022.2072554","url":null,"abstract":"ABSTRACT The study’s aim was to investigate the S100A4-mediated mechanisms of the regulation of tumor cell proliferation and migration in the human triple-positive breast carcinoma cell line MCF-7 (TPBC) and triple-negative breast carcinoma cell line MDA-MB-231 (TNBC). The proliferative activity of TNBC more than doubled during the incubation in the conditioned medium of TPBC. Extracellular S100A4 dose-dependently decreased the proliferative response of TPBC. TPBC negatively impacted the growth of TNBCs during their co-culturing. TPBC significantly decreased the migration activity of the TNBC cells while the S100A4 intracellular level in the TNBC was also decreasing. The decrease in the S100A4 intracellular level occurred due to the protein’s monomeric form while the contribution of the dimeric form into the overall S100A4 concentration in TNBC cells increased 1.5-2-fold. The S100A4 pathway in the intercellular communication between TNBC and TPBCs also included the dexamethasone-sensitive mechanisms of S100A4 intra- and extracellular pools regulation.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49213300","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":"Analysis of exosome-derived microRNAs reveals insights of intercellular communication during invasion of breast, prostate and glioblastoma cancer cells.","authors":"Francesca Lessi,&nbsp;Paolo Aretini,&nbsp;Milena Rizzo,&nbsp;Mariangela Morelli,&nbsp;Michele Menicagli,&nbsp;Sara Franceschi,&nbsp;Chiara Maria Mazzanti","doi":"10.1080/19336918.2021.1935407","DOIUrl":"10.1080/19336918.2021.1935407","url":null,"abstract":"<p><p>MiRNAs represent a mechanism that regulates gene expression in many pathological conditions. Exosomes are known to be secreted from all types of cells, and the exosomes-released molecules are crucial messengers that can regulate cellular processes. We investigated the miRNAs content of exosomes released by cancer cells during the invasion . An invasion stimulus has been generated through scratches created on the confluent cells of cancer cell lines: glioblastoma, breast and prostate cancers.Several miRNAs were found to be significantly differentially abundant during the cell invasion , both in common among different cell lines and exclusive. Understanding the language codes among cells involved in invasion can lead to the development of therapies that can inhibit cellular communication, slowing or eventually stopping their activity.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1935407","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39097492","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":"P21-activated kinase regulates oxygen-dependent migration of vascular endothelial cells in monolayers.","authors":"Satomi Hirose,&nbsp;Yugo Tabata,&nbsp;Kazuki Sone,&nbsp;Naoyuki Takahashi,&nbsp;Daisuke Yoshino,&nbsp;Kenichi Funamoto","doi":"10.1080/19336918.2021.1978368","DOIUrl":"https://doi.org/10.1080/19336918.2021.1978368","url":null,"abstract":"<p><p>The collective migration of vascular endothelial cells plays important roles in homeostasis and angiogenesis. Oxygen concentration <i>in vivo</i>, which is lower than in the atmosphere and changes due to diseases, is a key factor affecting the cellular dynamics of vascular endothelial cells. We previously reported that hypoxic conditions promote the internalization of vascular endothelial (VE)-cadherin, a specific cell-cell adhesion molecule, and increase the velocity of the collective migration of vascular endothelial cells. However, the mechanism through which cells regulate collective migration as affected by oxygen tension is not fully understood. Here, we investigated oxygen-dependent collective migration, focusing on intracellular protein p21-activated kinase (PAK) and hypoxia-inducing factor (HIF)-1α. A monolayer of human umbilical vein vascular endothelial cells (HUVECs) was formed in a microfluidic device with controllability of oxygen tension. The HUVECs were then exposed to various oxygen conditions in a range from 0.8% to 21% O₂, with or without PAK inhibition or chemical stabilization of HIF-1α. Collective cell migration was measured by particle image velocimetry with time-lapse phase-contrast microscopic images. Localizations of VE-cadherin and HIF-1α were quantified by immunofluorescent staining. The collective migration of HUVECs varied in an oxygen-dependent fashion; the migration speed was increased by hypoxic exposure down to 1% O₂, while it decreased under an extremely low oxygen tension of less than 1% O₂. PAK inhibition suppressed the hypoxia-induced increase of the migration speed by preventing VE-cadherin internalization into HUVECs. A decrease in the migration speed was also obtained by chemical stabilization of HIF-1α, suggesting that excessive accumulation of HIF-1α diminishes collective cell migration. These results indicate that the oxygen-dependent variation of the migration speed of vascular endothelial cells is mediated by the regulation of VE-cadherin through the PAK pathway, as well as other mechanisms via HIF-1α, especially under extreme hypoxic conditions.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8475594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39437794","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":"Role of laminin and cognate receptors in cholangiocarcinoma cell migration.","authors":"Kittiya Islam,&nbsp;Parichut Thummarati,&nbsp;Pakkanun Kaewkong,&nbsp;Banchob Sripa,&nbsp;Tuangporn Suthiphongchai","doi":"10.1080/19336918.2021.1924422","DOIUrl":"https://doi.org/10.1080/19336918.2021.1924422","url":null,"abstract":"<p><p>Extensive desmoplasia in cholangiocarcinoma (CCA) is associated with tumor aggressiveness, indicating a need for further understanding of CCA cell-matrix interaction. This study demonstrated laminin as the most potent attractant for CCA cell migration and the vast elevation of its receptor integrin β4 (ITGB4) in CCA cell lines. Besides, their high expressions in CCA tissues were correlated with lymphatic invasion and the presence of ITGB4 was also associated with short survival time. ITGB4 silencing revealed it as the receptor for laminin-induced HuCCA-1 migration, but KKU-213 utilized 37/67-kDa laminin receptor (LAMR) instead. These findings highlight the role of ITGB4 and LAMR in transducing laminin induction of CCA cell migration and the potential of ITGB4 as diagnostic and prognostic biomarkers for CCA.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1924422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39000750","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":"A role for GLUT3 in glioblastoma cell invasion that is not recapitulated by GLUT1.","authors":"Catherine J Libby,&nbsp;Sajina Gc,&nbsp;Gloria A Benavides,&nbsp;Jennifer L Fisher,&nbsp;Sarah E Williford,&nbsp;Sixue Zhang,&nbsp;Anh Nhat Tran,&nbsp;Emily R Gordon,&nbsp;Amber B Jones,&nbsp;Kaysaw Tuy,&nbsp;William Flavahan,&nbsp;Juan Gordillo,&nbsp;Ashlee Long,&nbsp;Sara J Cooper,&nbsp;Brittany N Lasseigne,&nbsp;Corinne E Augelli-Szafran,&nbsp;Victor Darley-Usmar,&nbsp;Anita B Hjelmeland","doi":"10.1080/19336918.2021.1903684","DOIUrl":"https://doi.org/10.1080/19336918.2021.1903684","url":null,"abstract":"<p><p>The multifaceted roles of metabolism in invasion have been investigated across many cancers. The brain tumor glioblastoma (GBM) is a highly invasive and metabolically plastic tumor with an inevitable recurrence. The neuronal glucose transporter 3 (GLUT3) was previously reported to correlate with poor glioma patient survival and be upregulated in GBM cells to promote therapeutic resistance and survival under restricted glucose conditions. It has been suggested that the increased glucose uptake mediated by GLUT3 elevation promotes survival of circulating tumor cells to facilitate metastasis. Here we suggest a more direct role for GLUT3 in promoting invasion that is not dependent upon changes in cell survival or metabolism. Analysis of glioma datasets demonstrated that GLUT3, but not GLUT1, expression was elevated in invasive disease. In human xenograft derived GBM cells, GLUT3, but not GLUT1, elevation significantly increased invasion in transwell assays, but not growth or migration. Further, there were no changes in glycolytic metabolism that correlated with invasive phenotypes. We identified the GLUT3 C-terminus as mediating invasion: substituting the C-terminus of GLUT1 for that of GLUT3 reduced invasion. RNA-seq analysis indicated changes in extracellular matrix organization in GLUT3 overexpressing cells, including upregulation of osteopontin. Together, our data suggest a role for GLUT3 in increasing tumor cell invasion that is not recapitulated by GLUT1, is separate from its role in metabolism and survival as a glucose transporter, and is likely broadly applicable since GLUT3 expression correlates with metastasis in many solid tumors.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1903684","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25580921","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":"MAGI1 localizes to mature focal adhesion and modulates endothelial cell adhesion, migration and angiogenesis.","authors":"Begoña Alday-Parejo,&nbsp;Kedar Ghimire,&nbsp;Oriana Coquoz,&nbsp;Gioele W Albisetti,&nbsp;Luca Tamò,&nbsp;Jelena Zaric,&nbsp;Jimmy Stalin,&nbsp;Curzio Rüegg","doi":"10.1080/19336918.2021.1911472","DOIUrl":"https://doi.org/10.1080/19336918.2021.1911472","url":null,"abstract":"<p><p>MAGI1 is an intracellular adaptor protein that stabilizes cell junctions and regulates epithelial and endothelial integrity. Here, we report that that in endothelial cells MAGI1 colocalizes with paxillin, β3-integrin, talin 1, tensin 3 and α-4-actinin at mature focal adhesions and actin stress fibers, and regulates their dynamics. Downregulation of MAGI1 reduces focal adhesion formation and maturation, cell spreading, actin stress fiber formation and RhoA/Rac1 activation. MAGI1 silencing increases phosphorylation of paxillin at Y118, an indicator of focal adhesion turnover. MAGI1 promotes integrin-dependent endothelial cells adhesion to ECM, reduces invasion and tubulogenesis<i>in vitro</i> and suppresses angiogenesis  <i>in vivo</i>. Our results identify MAGI1 as anovel component of focal adhesions, and regulator of focal adhesion dynamics, cell adhesion, invasion and angiogenesis.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1911472","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25565481","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":"Tissue factor potentiates adherence of breast cancer cells to human umbilical vein endothelial cells under static and flow conditions.","authors":"Yanling Jin,&nbsp;Wei Liu,&nbsp;Fengxia Wang,&nbsp;Min Wang,&nbsp;Kai Xu,&nbsp;Aijun Yang,&nbsp;Chenyu Wang,&nbsp;Lihan Zhang,&nbsp;Fangfang Zhang,&nbsp;Min Li","doi":"10.1080/19336918.2021.1898709","DOIUrl":"https://doi.org/10.1080/19336918.2021.1898709","url":null,"abstract":"<p><p>Tissue factor (TF) has been extensively studied for tumor metastasis, but its role in mediating cancer cell adhesion to vasculature remains unknown. This study aimed to measure the ability of TF to mediate the adhesion of breast cancer cells to human umbilical vein endothelial cells (HUVECs). MDA-MB-231 cells expressed the highest TF level and adhered more to HUVECs under static and flow conditions, a neutralizing TF antibody abolished the enhanced adhesion of MDA-MB-231 cells to HUVECs. Recombinant human soluble TF (rTF) bonded β1integrin on HUVECs surfaces, β1 or α3integrin antibody combined with TF antibody abolished more cell-cell adhesion. These data suggested that TF mediated adhesion of breast cancer cells to endothelial cells may rely on β1integrin on HUVECs surfaces.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2021.1898709","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25500666","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}