Deborah J Wessels, Claude Pujol, Nikash Pradhan, Daniel F Lusche, Luis Gonzalez, Sydney E Kelly, Elizabeth M Martin, Edward R Voss, Yang-Nim Park, Michael Dailey, Sonia L Sugg, Sneha Phadke, Amani Bashir, David R Soll
{"title":"Directed movement toward, translocation along, penetration into and exit from vascular networks by breast cancer cells in 3D.","authors":"Deborah J Wessels, Claude Pujol, Nikash Pradhan, Daniel F Lusche, Luis Gonzalez, Sydney E Kelly, Elizabeth M Martin, Edward R Voss, Yang-Nim Park, Michael Dailey, Sonia L Sugg, Sneha Phadke, Amani Bashir, David R Soll","doi":"10.1080/19336918.2021.1957527","DOIUrl":"https://doi.org/10.1080/19336918.2021.1957527","url":null,"abstract":"<p><p>We developed a computer-assisted platform using laser scanning confocal microscopy to 3D reconstruct in real-time interactions between metastatic breast cancer cells and human umbilical vein endothelial cells (HUVECs). We demonstrate that MB-231 cancer cells migrate toward HUVEC networks, facilitated by filopodia, migrate along the network surfaces, penetrate into and migrate within the HUVEC networks, exit and continue migrating along network surfaces. The system is highly amenable to 3D reconstruction and computational analyses, and assessments of the effects of potential anti-metastasis monoclonal antibodies and other drugs. We demonstrate that an anti-RHAMM antibody blocks filopodium formation and all of the behaviors that we found take place between MB-231 cells and HUVEC networks.</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/10.1080/19336918.2021.1957527","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39267512","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":"Nicotinate-curcumin inhibits AngII-induced vascular smooth muscle cell phenotype switching by upregulating Daxx expression.","authors":"Si-Yu Sun, Yu-Mei Cao, Yan-Jie Huo, Fei Qiu, Wen-Juan Quan, Chao-Ping He, Yu Chen, Duan-Fang Liao, Qin-Hui Tuo","doi":"10.1080/19336918.2021.1909899","DOIUrl":"https://doi.org/10.1080/19336918.2021.1909899","url":null,"abstract":"<p><p>Phenotypic switching is the main cause of the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs). We previously showed that Daxx exerted negative regulatory effect on AngII-induced VSMC proliferation and migration. However, the function of Daxx in VSMC phenotype switching remained unknown. Nicotinate-curcumin (NC) is an esterification derivative of niacin and curcumin that can prevent the formation of atherosclerosis. We found that NC significantly decreased AngII-induced VSMC phenotype switching. Furthermore, NC significantly inhibited AngII-induced cell proliferation and migration. Moreover, NC upregulated Daxx expression and regulated the PTEN/Akt signaling pathway. We concluded that NC inhibited AngII-induced VSMC phenotype switching by regulating the PTEN/Akt pathway, and through a mechanism that might be associated with the upregulation of Daxx expression.</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/10.1080/19336918.2021.1909899","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25599352","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}
Francesco Roncato, Ofer Regev, Sandeep Kumar Yadav, Ronen Alon
{"title":"Microtubule destabilization is a critical checkpoint of chemotaxis and transendothelial migration in melanoma cells but not in T cells.","authors":"Francesco Roncato, Ofer Regev, Sandeep Kumar Yadav, Ronen Alon","doi":"10.1080/19336918.2021.1934958","DOIUrl":"https://doi.org/10.1080/19336918.2021.1934958","url":null,"abstract":"<p><p>Microtubules (MTs) control cell shape and intracellular cargo transport. The role of MT turnover in the migration of slow-moving cells through endothelial barriers remains unclear. To irreversibly interfere with MT disassembly, we have used the MT-stabilizing agent zampanolide (ZMP) in Β16F10 melanoma as amodel of slow-moving cells. ZMP-treated B16 cells failed to follow chemotactic gradients across rigid confinements and could not generate stable sub-endothelial pseudopodia under endothelial monolayers. In vivo, ZMP-treated Β16 cells failed to extravasate though lung capillaries. In contrast to melanoma cells, the chemotaxis and transendothelial migration of ZMP-treated Tcells were largely conserved. This is afirst demonstration that MT disassembly is akey checkpoint in the directional migration of cancer cells but not of lymphocytes.</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/10.1080/19336918.2021.1934958","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39252968","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}
Wishrawana S Ratnayake, Christopher A Apostolatos, Sloan Breedy, Clare L Dennison, Robert Hill, Mildred Acevedo-Duncan
{"title":"Atypical PKCs activate Vimentin to facilitate prostate cancer cell motility and invasion.","authors":"Wishrawana S Ratnayake, Christopher A Apostolatos, Sloan Breedy, Clare L Dennison, Robert Hill, Mildred Acevedo-Duncan","doi":"10.1080/19336918.2021.1882782","DOIUrl":"https://doi.org/10.1080/19336918.2021.1882782","url":null,"abstract":"<p><p>Atypical protein kinase C (aPKC) are involved in progression of many human cancers. Vimentin is expressed during epithelial to mesenchymal transition (EMT). Molecular dynamics of Vimentin intermediate filaments (VIFs) play a key role in metastasis. This article is an effort to provide thorough understanding of the relationship between Vimentin and aPKCs . We demonstrate that diminution of aPKCs lead to attenuate prostate cellular metastasis through the downregulation of Vimentin expression. <i>si</i>RNA knocked-down SNAIL1 and PRRX1 reduce aPKC activity along with Vimentin. Results suggest that aPKCs target multiple activation sites (Ser33/39/56) on Vimentin and therefore is essential for VIF dynamics regulation during the metastasis of prostate cancer cells. Understanding the aPKC related molecular mechanisms may provide a novel therapeutic path for prostate carcinoma.</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/10.1080/19336918.2021.1882782","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25319752","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}
Kateřina Kuželová, Adam Obr, Pavla Röselová, Dana Grebeňová, Petra Otevřelová, Barbora Brodská, Aleš Holoubek
{"title":"Group I p21-activated kinases in leukemia cell adhesion to fibronectin.","authors":"Kateřina Kuželová, Adam Obr, Pavla Röselová, Dana Grebeňová, Petra Otevřelová, Barbora Brodská, Aleš Holoubek","doi":"10.1080/19336918.2021.1872760","DOIUrl":"https://doi.org/10.1080/19336918.2021.1872760","url":null,"abstract":"<p><p>P21-activated kinases (PAK) regulate processes associated with cytoskeleton dynamics. PAK expression in leukemia cells was measured on protein and mRNA levels. In functional assays, we analyzed the effect of PAK inhibitors IPA-3 and FRAX597 on cell adhesivity and viability. PAK2 was dominant in cell lines, whereas primary cells also expressed comparable amount of PAK1 transcription isoforms: PAK1-full and PAK1Δ15. PAK1Δ15 and PAK2 levels correlated with surface density of integrins β1 and αVβ3. PAK1-full, but not PAK2, was present in membrane protrusions. IPA-3, which prevents PAK activation, induced cell contraction in semi-adherent HEL cells only. FRAX597, which inhibits PAK kinase activity, increased cell-surface contact area in all leukemia cells. Both inhibitors reduced the stability of cell attachment and induced cell death.</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/10.1080/19336918.2021.1872760","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38768449","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":"F4, a collagen XIX-derived peptide, inhibits tumor angiogenesis through αvβ3 and α5β1 integrin interaction.","authors":"Jean-Baptiste Oudart, Matthieu Villemin, Bertrand Brassart, Christèle Sellier, Christine Terryn, Aurélie Dupont-Deshorgue, Jean Claude Monboisse, François-Xavier Maquart, Laurent Ramont, Sylvie Brassart-Pasco","doi":"10.1080/19336918.2021.1951425","DOIUrl":"https://doi.org/10.1080/19336918.2021.1951425","url":null,"abstract":"<p><p>We previously demonstrated that F4 peptide (CNPEDCLYPVSHAHQR) from collagen XIX was able to inhibit melanoma cell migration<i>in vitro</i> and cancer progression in a mouse melanoma model. The aim of the present work was to study the anti-angiogenic properties of F4 peptide. We demonstrated that F4 peptide inhibited VEGF-induced pseudo-tube formation on Matrigel by endothelial cells and endothelial sprouting in a rat aortic ring assay. By affinity chromatography, we identified αvβ3 and α5β1 integrins as potential receptors for F4 peptide on endothelial cell surface. Using solid phase assays, we proved the direct interaction between F4 and both integrins. Taken together, our results demonstrate that F4 peptide is a potent antitumor agent inhibiting both angiogenesis and tumor cell migration.</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/10.1080/19336918.2021.1951425","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39222301","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}
Andrea A Villanueva, Pilar Sanchez-Gomez, Ernesto Muñoz-Palma, Sofía Puvogel, Bárbara S Casas, Cecilia Arriagada, Isaac Peña-Villalobos, Pablo Lois, Manuel Ramírez Orellana, Fabiana Lubieniecki, Fernando Casco Claro, Iván Gallegos, Javier García-Castro, Vicente A Torres, Verónica Palma
{"title":"The Netrin-1-Neogenin-1 signaling axis controls neuroblastoma cell migration via integrin-β1 and focal adhesion kinase activation.","authors":"Andrea A Villanueva, Pilar Sanchez-Gomez, Ernesto Muñoz-Palma, Sofía Puvogel, Bárbara S Casas, Cecilia Arriagada, Isaac Peña-Villalobos, Pablo Lois, Manuel Ramírez Orellana, Fabiana Lubieniecki, Fernando Casco Claro, Iván Gallegos, Javier García-Castro, Vicente A Torres, Verónica Palma","doi":"10.1080/19336918.2021.1892397","DOIUrl":"10.1080/19336918.2021.1892397","url":null,"abstract":"<p><p>Neuroblastoma is a highly metastatic tumor that emerges from neural crest cell progenitors. Focal Adhesion Kinase (FAK) is a regulator of cell migration that binds to the receptor Neogenin-1 and is upregulated in neuroblastoma. Here, we show that Netrin-1 ligand binding to Neogenin-1 leads to FAK autophosphorylation and integrin β1 activation in a FAK dependent manner, thus promoting neuroblastoma cell migration. Moreover, Neogenin-1, which was detected in all tumor stages and was required for neuroblastoma cell migration, was found in a complex with integrin β1, FAK, and Netrin-1. Importantly, Neogenin-1 promoted neuroblastoma metastases in an immunodeficient mouse model. Taken together, these data show that Neogenin-1 is a metastasis-promoting protein that associates with FAK, activates integrin β1 and promotes neuroblastoma cell migration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7971226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25483843","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":"α- Linolenic acid modulates phagocytosis and endosomal pathways of extracellular Tau in microglia.","authors":"Smita Eknath Desale, Subashchandrabose Chinnathambi","doi":"10.1080/19336918.2021.1898727","DOIUrl":"10.1080/19336918.2021.1898727","url":null,"abstract":"<p><p>Microglia, the resident immune cells, were found to be activated to inflammatory phenotype in Alzheimer's disease (AD). The extracellular burden of amyloid-β plaques and Tau seed fabricate the activation of microglia. The seeding effect of extracellular Tau species is an emerging aspect to study about Tauopathies in AD. Tau seeds enhance the propagation of disease along with its contribution to microglia-mediated inflammation. The excessive neuroinflammation cumulatively hampers phagocytic function of microglia reducing the clearance of extracellular protein aggregates. Omega-3 fatty acids, especially docosahexaenoic acid and eicosapentaenoic acid, are recognized to induce anti-inflammatory phenotype of microglia. In addition to increased cytokine production, omega-3 fatty acids enhance phagocytic receptors expression in microglia. In this study, we have observed the phagocytosis of extracellular Tau in the presence of α-linolenic acid (ALA). The increased phagocytosis of extracellular Tau monomer and aggregates have been observed upon ALA exposure to microglia cells. After internalization, the degradation status of Tau has been studied with early and late endosomal markers Rab5 and Rab7. Further, the lysosome-mediated degradation of internalized Tau was studied with LAMP-2A, a lysosome marker. The enhanced migratory ability in the presence of ALA could be beneficial for microglia to access the target and clear it. The increased migration of microglia was found to induce the microtubule-organizing center repolarization. The data indicate that the dietary fatty acids ALA could significantly enhance phagocytosis and intracellular degradation of internalized Tau. Our results suggest that microglia could be influenced to reduce extracellular Tau seed with dietary fatty acids.</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/10.1080/19336918.2021.1898727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25492209","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}
Sofia Mogren, Frida Berlin, Sangeetha Ramu, Asger Sverrild, Celeste Porsbjerg, Lena Uller, Cecilia K Andersson
{"title":"Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells.","authors":"Sofia Mogren, Frida Berlin, Sangeetha Ramu, Asger Sverrild, Celeste Porsbjerg, Lena Uller, Cecilia K Andersson","doi":"10.1080/19336918.2021.1950594","DOIUrl":"https://doi.org/10.1080/19336918.2021.1950594","url":null,"abstract":"<p><p>Epithelial damage and increase of intraepithelial mast cells (MC) are characteristics of asthma. The role of MC mediator tryptase and the protease-activated receptor-2 (PAR2) on epithelial wound healing is not fully investigated. Stimulation of bronchial epithelial cells (BECs) with tryptase promoted gap closure, migration and cellular speed compared to controls. Stimulated BECs had higher expression of migration marker CD151 compared to controls. Proliferation marker KI67 was upregulated in tryptase-stimulated BECs compared to controls. Treatment with PAR2 antagonist I-191 reduced gap closure, migration and cell speed compared to BECs stimulated with tryptase. We found that tryptase enhances epithelial wound healing by increased migration and proliferation, which is in part regulated via PAR2. Our data suggest that tryptase might be beneficial in tissue repair under baseline conditions. However, in a pathological context such as asthma with increased numbers of activated MCs, it might lead to epithelial remodeling and loss of function.</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/10.1080/19336918.2021.1950594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39221709","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":"Long noncoding RNA <i>ENST00000508435</i> promotes migration of breast cancer via FXR 1.","authors":"Luying Li, Youping Jin, Xue Wang, Li Wang, Yangbai Sun, Yihong Luo, Xiaojian Ni, Qi Lu, Wenbo Wei, Xiuling Zhi, Jerry Yu, Wei Zhu, Ping Zhou","doi":"10.1080/19336918.2021.1921402","DOIUrl":"https://doi.org/10.1080/19336918.2021.1921402","url":null,"abstract":"<p><p>LncRNA plays a critical role in tumor progression. However, the role it executes in breast cancer is still unclear. Here, we report a newly discovered lncRNA, <i>ENST00000508435</i>, which could be remarkably up-regulated in breast cancer cells and tissues. We found that the expression of <i>ENST00000508435</i> was positively correlated with tumor size, lymph node metastasis and HER2. More interesting, overexpression of <i>ENST00000508435</i> significantly increased cell migration, while specific knockdown led to the opposite. RNA pull-down and RNA immunoprecipitation assays demonstrated that <i>ENST00000508435</i> could directly bind to FXR1 to promote tumor metastasis. <i>ENST00000508435</i> and FXR1 were positively correlated. FXR1 was also significantly up-regulated in breast tumors. Taken together, we propose that <i>ENST00000508435</i> regulates FXR1 to promote breast cancer metastasis.</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/10.1080/19336918.2021.1921402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38955206","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}