Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2018-08-19DOI: 10.1080/19336918.2018.1491234
Cecilia Arriagada, Patricio Silva, Vicente A Torres
{"title":"Role of glycosylation in hypoxia-driven cell migration and invasion.","authors":"Cecilia Arriagada, Patricio Silva, Vicente A Torres","doi":"10.1080/19336918.2018.1491234","DOIUrl":"https://doi.org/10.1080/19336918.2018.1491234","url":null,"abstract":"<p><p>Hypoxia, a common condition of the tumor microenvironment, induces changes in the proteome of cancer cells, mainly via HIF-1, a transcription factor conformed by a constitutively expressed β-subunit and an oxygen-regulated α-subunit. In hypoxia, HIF-1α stabilizes, forms the heterodimeric complex with HIF-1β, and binds to Hypoxia Response Elements (HRE), activating gene expression to promote metabolic adaptation, cell invasion and metastasis. Furthermore, the focal adhesion kinase, FAK, is activated in hypoxia, promoting cell migration by mechanisms that remain unclear. In this context, integrins, which are glycoproteins required for cell migration, are possibly involved in hypoxia-induced FAK activation. Evidence suggests that cancer cells have an altered glycosylation metabolism, mostly by the expression of glycosyltransferases, however the relevance of glycosylation is poorly explored in the context of hypoxia. Here, we discuss the role of hypoxia in cancer, and its effects on protein glycosylation, with emphasis on integrins and cell migration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"13-22"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1491234","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36317592","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 : 2019-12-01Epub Date: 2018-11-18DOI: 10.1080/19336918.2018.1546513
S M Anisul Islam, Rekha Patel, Raja Reddy Bommareddy, Khandker Mohammad Khalid, Mildred Acevedo-Duncan
{"title":"The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells.","authors":"S M Anisul Islam, Rekha Patel, Raja Reddy Bommareddy, Khandker Mohammad Khalid, Mildred Acevedo-Duncan","doi":"10.1080/19336918.2018.1546513","DOIUrl":"https://doi.org/10.1080/19336918.2018.1546513","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most common cancer in the United States. The exact mechanism of CRC cells metastasis is poorly understood. Actin polymerization is thought to be an initial step in the cancer cell motility cycle which drives the formation of cell protrusions and defines the direction of migration. Cofilin, a significant actin-regulating molecule, regulates the migration of cancer cells by the formation of lamellipodia and filopodia, however, little is known about the upstream regulation of cofilin. In this study, the effect of atypical Protein Kinase C (atypical PKC) on Cofilin activity in CRC was studied. This study demonstrates that the atypical PKC inhibition impedes the metastasis of CRC cells by increasing phospho-Cofilin (S3) and changing actin organization.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"106-120"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1546513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36715454","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 : 2019-12-01Epub Date: 2019-03-17DOI: 10.1080/19336918.2019.1587269
Nicholas R Anderson, Alexander Buffone, Daniel A Hammer
{"title":"T lymphocytes migrate upstream after completing the leukocyte adhesion cascade.","authors":"Nicholas R Anderson, Alexander Buffone, Daniel A Hammer","doi":"10.1080/19336918.2019.1587269","DOIUrl":"https://doi.org/10.1080/19336918.2019.1587269","url":null,"abstract":"<p><p>The leukocyte adhesion cascade is of critical importance for both the maintenance of immune homeostasis and the ability of immune cells to perform effector functions. Here, we present data showing CD4<sup>+</sup> T cells migrate upstream (against the direction of flow) after completing the leukocyte adhesion cascade on surfaces displaying either ICAM-1 or ICAM-1 and VCAM-1, but migrate downstream on surfaces displaying only VCAM-1. Cells completing the cascade on HUVECs initially migrate upstream before reverting to more random migration, partly caused by transmigration of cells migrating against the flow. Furthermore, cells migrating upstream transmigrate faster than cells migrating downstream. On HUVECs, blocking interactions between LFA-1 and ICAM-1 resulted in downstream migration and slower transmigration. These results further suggest a possible physiological role for upstream migration in vivo.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"163-168"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1587269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37063939","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":"Protein kinase C Inhibitors selectively modulate dynamics of cell adhesion molecules and cell death in human colon cancer cells.","authors":"Muzaffer Dükel, Zehra Tavsan, Duygu Erdogan, Deniz Erkan Gök, Hulya Ayar Kayali","doi":"10.1080/19336918.2018.1530933","DOIUrl":"https://doi.org/10.1080/19336918.2018.1530933","url":null,"abstract":"<p><p>During development of colon cancer, Protein Kinase Cs (PKCs) are involved in regulation of many genes controlling several cellular mechanisms. Here, we examined the changes in cell adhesion molecules and PKCs for colorectal cancer progression. We identified that PKCs affected expression of EpCAM, claudins, tetraspanins. Treatment with low concentrations of PKC inhibitors resulted in decreased cell viability. In addition, immunoblotting and qRT-PCR analysis showed that apoptosis was inhibited while autophagy was induced by PKC inhibition in colon cancer cells. Furthermore, we observed decreased levels of intracellular Reactive Oxygen Species (ROS), lipid peroxidation and protein carbonyl, confirming the ROS-induced apoptosis. Taken together, our results reveal that PKC signalling modulates not only cell adhesion dynamics but also cell death-related mechanisms. Abbreviations: PKC: Protein Kinase C; EpCAM: Epithelial cell adhesion molecule; FBS: fetal bovine serum; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide); CAM: cell adhesion molecule; ROS: reactive oxygen species.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"83-97"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1530933","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36559873","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}
S. Cejkova, H. Kubátová, F. Thieme, L. Janousek, J. Fronek, R. Poledne, I. Králová Lesná
{"title":"The effect of cytokines produced by human adipose tissue on monocyte adhesion to the endothelium","authors":"S. Cejkova, H. Kubátová, F. Thieme, L. Janousek, J. Fronek, R. Poledne, I. Králová Lesná","doi":"10.1080/19336918.2019.1644856","DOIUrl":"https://doi.org/10.1080/19336918.2019.1644856","url":null,"abstract":"ABSTRACT Visceral adipose tissue (VAT) may play a critical role in atherosclerotic cardiovascular disease. The goal of this study was to determine the effect of human VAT-released pro‑inflammatory cytokines on monocyte adhesion to the endothelium. The cytokine effects on monocyte adhesion to the endothelial cells (ECs) were tested using adipose tissue-conditioned media (ATCM) prepared by culturing human VAT. The cytokines concentrations in ATCM, the cytokines expression and adhesion molecules in stimulated ECs were measured. The concentrations of IL-1β,TNF-α,MCP-1,IL-10,and RANTES measured in ATCM correlated positively with monocyte adhesiveness to ECs. Additionally, ATCM increased the adhesion molecules (ICAM-1, VCAM-1) gene expression. Selective inhibitors highlighted the importance of IL-1β and TNF-α in the process by a significant decrease in monocyte adhesion compared to ATCM preconditioning without inhibitors. Human VAT significantly increased monocyte adhesion to ECs. It was significantly influenced by IL-1β, TNF-α, MCP-1, IL-10, and RANTES, with IL-1β and TNF‑α having the strongest impact.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"293 - 302"},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1644856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43935771","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":"Splicing factor-modulated generation of mechano growth factor regulates physiological processes in osteoblasts under mechanical stimuli","authors":"Qian Yi, Huan Liu, Jianguo Feng, Yanjiao Wu, Weichao Sun, Mengting Ou, Liling Tang","doi":"10.1080/19336918.2019.1686103","DOIUrl":"https://doi.org/10.1080/19336918.2019.1686103","url":null,"abstract":"ABSTRACT Mechanical stimuli influence various physiological processes in osteoblasts. We previously showed that mechano-growth factor (MGF), a splicing variant of insulin-like growth factor 1, is highly expressed in osteoblasts in response to mechanical stimuli. This study aims to explore the systemic functions of MGF in osteoblasts, and the mechanisms by which mechanical stress regulates the alternative splicing of Igf1 to generate MGF. We found that MGF promoted the proliferation and migration of osteoblasts, while it inhibited their differentiation via Erk1/2 pathway. Furthermore, cyclic stretching upregulated the expression of ASF/SF2, which in turn regulated the expression of MGF. Our findings indicate that mechanical stimuli influence the physiological responses of osteoblasts by increasing the expression of MGF, which is regulated by splicing factors.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"322 - 331"},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1686103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41395646","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}
H. B. Mangukiya, H. Negi, S. B. Merugu, Qudsia Sehar, D. S. Mashausi, F. Yunus, Zhenghua Wu, Dawei Li
{"title":"Paracrine signalling of AGR2 stimulates RhoA function in fibroblasts and modulates cell elongation and migration","authors":"H. B. Mangukiya, H. Negi, S. B. Merugu, Qudsia Sehar, D. S. Mashausi, F. Yunus, Zhenghua Wu, Dawei Li","doi":"10.1080/19336918.2019.1685928","DOIUrl":"https://doi.org/10.1080/19336918.2019.1685928","url":null,"abstract":"ABSTRACT The most prominent cancer-associated fibroblasts (CAFs) in tumor stroma is known to form a protective structure to support tumor growth. Anterior gradient-2 (AGR2), a tumor secretory protein is believed to play a pivotal role during tumor microenvironment (TME) development. Here, we report that extracellular AGR2 enhances fibroblasts elongation and migration significantly. The early stimulation of RhoA showed the association of AGR2 by upregulation of G1-S phase-regulatory protein cyclin D1 and FAK phosphorylation through fibroblasts growth factor receptor (FGFR) and vascular endothelial growth factor receptor (VEGFR). Our finding indicates that secretory AGR2 alters fibroblasts elongation, migration, and organization suggesting the secretory AGR2 as a potential molecular target that might be responsible to alter fibroblasts infiltration to support tumor growth.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"332 - 344"},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1685928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47123853","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}
Melville B Vaughan, Gang Xu, Tracy L. Morris, Pratiksha Kshetri, Jing X Herwig
{"title":"Predictable fibroblast tension generation by measuring compaction of anchored collagen matrices using microscopy and optical coherence tomography","authors":"Melville B Vaughan, Gang Xu, Tracy L. Morris, Pratiksha Kshetri, Jing X Herwig","doi":"10.1080/19336918.2019.1644855","DOIUrl":"https://doi.org/10.1080/19336918.2019.1644855","url":null,"abstract":"ABSTRACT The anchored fibroblast-populated collagen matrix (aFPCM) is an appropriate model to study fibrocontractive disease mechanisms. Our goal was to determine if aFPCM height reduction (compaction) during development is sufficient to predict tension generation. Compaction was quantified daily by both traditional light microscopy and an optical coherence tomography (OCT) system. Contraction in aFPCM was revealed by releasing them from anchorage. We found that aFPCM contraction increase was correlated to the compaction increase. Cytochalasin D treatment reversibly inhibited compaction. Therefore, we demonstrated that aFPCM height reduction efficiently measures compaction, contraction, and relative maturity of the collagen matrix during development or treatment. In addition, we showed that OCT is suitable for effectively imaging the cross-sectional morphology of the aFPCM in culture. This study will pave the way for more efficient studies on the mechanisms of (and treatments that target) migration and contraction in wound healing and Dupuytren’s contracture in a tissue environment.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"303 - 314"},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1644855","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45978409","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":"Mathematical Models of Specific Cell Adhesion Phenomena","authors":"M. Hjortso, J. Roos","doi":"10.1201/9781315138954-2","DOIUrl":"https://doi.org/10.1201/9781315138954-2","url":null,"abstract":"","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"38 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2018-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90907012","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":"Kinetics of Ligand-Receptor Bond Formation","authors":"J. Roos, M. Hjortso","doi":"10.1201/9781315138954-1","DOIUrl":"https://doi.org/10.1201/9781315138954-1","url":null,"abstract":"","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"29 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2018-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74333357","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}