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Structure, regulatory factors and cancer-related physiological effects of ADAM9. ADAM9的结构、调控因子及肿瘤相关生理作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1817251
M A Haoyuan, L I Yanshu
{"title":"Structure, regulatory factors and cancer-related physiological effects of ADAM9.","authors":"M A Haoyuan,&nbsp;L I Yanshu","doi":"10.1080/19336918.2020.1817251","DOIUrl":"https://doi.org/10.1080/19336918.2020.1817251","url":null,"abstract":"<p><p>The ADAMs family belongs to the transmembrane protein superfamily of zinc-dependent metalloproteases, which consists of multiple domains. These domains have independent but complementary functions that enable them to participate in multiple biological processes. Among them, ADAM9 can not only participate in the degradation of extracellular matrix as a metalloprotease, but also mediate tumor cell adhesion through its deintegrin domain, which is closely related to tumor invasion and metastasis. It is widely expressed in a variety of tumor cells and can affect the proliferation, invasion and metastasis of related cancer cells. We provide our views on current progress, its increasing importance as a strategic treatment goal, and our vision for the future of ADAM9.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"165-181"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1817251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38335795","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: 4
MicroRNA-203 inhibits epithelial-mesenchymal transition, migration, and invasion of renal cell carcinoma cells via the inactivation of the PI3K/AKT signaling pathway by inhibiting CAV1. MicroRNA-203通过抑制CAV1，使PI3K/AKT信号通路失活，从而抑制肾癌细胞的上皮-间质转化、迁移和侵袭。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1827665
Ning Han, Hai Li, Hui Wang
{"title":"MicroRNA-203 inhibits epithelial-mesenchymal transition, migration, and invasion of renal cell carcinoma cells via the inactivation of the PI3K/AKT signaling pathway by inhibiting CAV1.","authors":"Ning Han,&nbsp;Hai Li,&nbsp;Hui Wang","doi":"10.1080/19336918.2020.1827665","DOIUrl":"https://doi.org/10.1080/19336918.2020.1827665","url":null,"abstract":"<p><p>The present study aimed to evaluate the underlying mechanism of microRNA-203 (miR-203) in renal cell carcinoma (RCC) involving the PI3K/AKT signaling pathway. The results revealed downregulated miR-203 and upregulated CAV1 in RCC tissues. Upregulated miR-203 and downregulated CAV1 increased E-cadherin expression and cell apoptosis, decreased β-catenin and N-cadherin expression and cell proliferation, migration and invasion, and blocked cell cycle entry. CAV1, a target gene of miR-203, decreased by up-regulated miR-203, and silencing CAV1 led to the inactivation of PI3K/AKT signaling pathway. In conclusion, our findings suggested that miR-203-mediated direct suppression of CAV1 inhibits EMT of RCC cells via inactivation of the PI3K/AKT signaling pathway.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"227-241"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1827665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38528317","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: 9
Effect arylamine N-acetyltransferase 1 on morphology, adhesion, migration, and invasion of MDA-MB-231 cells: role of matrix metalloproteinases and integrin αV. 芳胺n -乙酰转移酶1对MDA-MB-231细胞形态、粘附、迁移和侵袭的影响:基质金属蛋白酶和整合素αV的作用
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2019.1710015
Pengcheng Li, Neville J Butcher, Rodney F Minchin
{"title":"Effect arylamine N-acetyltransferase 1 on morphology, adhesion, migration, and invasion of MDA-MB-231 cells: role of matrix metalloproteinases and integrin αV.","authors":"Pengcheng Li,&nbsp;Neville J Butcher,&nbsp;Rodney F Minchin","doi":"10.1080/19336918.2019.1710015","DOIUrl":"https://doi.org/10.1080/19336918.2019.1710015","url":null,"abstract":"<p><p>Reducted arylamine N-acetyltransferase (NAT1) in breast cancers is associated with poor patient survival. NAT1 has also been associated with changes in cancer cell survival and invasion both <i>in</i><i>vitro</i> and <i>in</i><i>vivo</i>. Here, we report the effects of NAT1 in cancer cell invasion by addressing its role in adherence, migration, and invasion <i>in vitro</i>. The NAT1 gene was deleted in MDA-MB-231, HT-29 and HeLa cells using CRISPR/Cas9 gene editing. Loss of NAT1 increased adherence to collagen in all three cell-lines but migration was unaffected. NAT1 deletion decreased invasion and induced changes to cell morphology. These effects were independent of matrix metalloproteinases but were related to integrin ITGαV expression. The data suggest NAT1 is important in adhesion and invasion through integrin expression.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1710015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37518425","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: 8
Thymol alleviates AGEs-induced podocyte injury by a pleiotropic effect via NF-κB-mediated by RhoA/ROCK signalling pathway. 百里香酚通过NF-κ b介导的RhoA/ROCK信号通路，通过多效性作用减轻age诱导的足细胞损伤。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1721172
Qinglian Wang, Zhenwei Shen, Guanghui Qi, Yanfang Zhao, Hongge Zhang, Rong Wang
{"title":"Thymol alleviates AGEs-induced podocyte injury by a pleiotropic effect via NF-κB-mediated by RhoA/ROCK signalling pathway.","authors":"Qinglian Wang,&nbsp;Zhenwei Shen,&nbsp;Guanghui Qi,&nbsp;Yanfang Zhao,&nbsp;Hongge Zhang,&nbsp;Rong Wang","doi":"10.1080/19336918.2020.1721172","DOIUrl":"https://doi.org/10.1080/19336918.2020.1721172","url":null,"abstract":"<p><p>Advanced glycation end products (AGE) are those of the most powerful pathogenic factors that related to diabetic complications. In our study, we investigated the beneficial effects of thymol on AGE induced cell injury and apoptosis in human podocytes (HPCs) and attempted to clarify its mechanisms. Our results revealed that stimulation with AGE could significantly activate RhoA/NF-κB pathway. Results showed thymol could markedly suppress inflammatory responses, cell apoptosis and disordered cytoskeleton. Also thymol restored the expression of podocin, restrained migration capacity. Western blot analysis indicated that it could restore the expression of RhoA, ROCK and vimentin, nephrin, podocin and p65 and IκBα phosphorylation. Moreover, si-RhoA also suppressed the expression of pro-inflammatory cytokines, ROCK, and vimentin and the phosphorylation of p65 and IκBα. In conclusion, thymol inhibits AGE-induced cell injury in HPCs by suppressing the RhoA-NF-κB pathway and may be apromising therapeutic agent.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"42-56"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1721172","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37618824","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: 8
BST2 regulates interferon gamma-dependent decrease in invasion of HTR-8/SVneo cells via STAT1 and AKT signaling pathways and expression of E-cadherin. BST2通过STAT1和AKT信号通路以及E-cadherin的表达调控干扰素γ依赖性的HTR-8/SVneo细胞侵袭减少。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2019.1710024
Sonam Verma, Amandeep Kaur Kang, Rahul Pal, Satish Kumar Gupta
{"title":"BST2 regulates interferon gamma-dependent decrease in invasion of HTR-8/SVneo cells via STAT1 and AKT signaling pathways and expression of E-cadherin.","authors":"Sonam Verma,&nbsp;Amandeep Kaur Kang,&nbsp;Rahul Pal,&nbsp;Satish Kumar Gupta","doi":"10.1080/19336918.2019.1710024","DOIUrl":"https://doi.org/10.1080/19336918.2019.1710024","url":null,"abstract":"<p><p>The mechanism by which interferon-gamma (IFN-γ) downregulates trophoblast invasion needs further investigation. Treatment of HTR-8/SVneo cells with IFN-γ led to a decrease in their invasion concomitant with an increased expression of BST2. Silencing of BST2 by siRNA showed a significant increase in their invasion and spreading after treatment with IFN-γ as well as downregulated expression of E-cadherin. Further, STAT1 silencing inhibited the IFN-γ-dependent increase in the expression of BST2 and E-cadherin. Treatment of HTR-8/SVneo cells with IFN-γ led to the activation of AKT, and its inhibition with PI3K inhibitor abrogated IFN-γ-mediated decrease in invasion/spreading and downregulated BST2 and E-cadherin expression. Collectively, IFN-γ decreases the invasion of HTR-8/SVneo cells by STAT1 and AKT activation via increased expression of BST2 and E-cadherin.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"24-41"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1710024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37560518","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: 7
Inhibition of DDR1 reduces invasive features of human A375 melanoma, HT29 colon carcinoma and SK-HEP hepatoma cells. 抑制DDR1可降低人类A375黑色素瘤、HT29结肠癌和SK-HEP肝癌细胞的侵袭性特征。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1733892
Irene Romayor, Iker Badiola, Elvira Olaso
{"title":"Inhibition of DDR1 reduces invasive features of human A375 melanoma, HT29 colon carcinoma and SK-HEP hepatoma cells.","authors":"Irene Romayor,&nbsp;Iker Badiola,&nbsp;Elvira Olaso","doi":"10.1080/19336918.2020.1733892","DOIUrl":"https://doi.org/10.1080/19336918.2020.1733892","url":null,"abstract":"<p><p>DDR1 is a receptor tyrosine kinases for collagen and an adverse prognostic factor in primary and metastatic tumors.Despite this, DDR1 signaling and its functional consequences in tumor development remain unclear. RT-PCR and Western blot show that A375, colon carcinoma HT29 and liver carcinoma SK-HEP human cell lines express functional DDR1 that phosphorylates in response to collagen type I. Chemical inhibition of DDR1 phosphorylation or DDR1 mRNA silencing reduced AKT and ERK phosphorylation, expression of ICAM1 and VCAM1, Ki67 and secretion of MMP9. DDR1 silenced cells showed reduced adhesion to collagen type I, MMP-dependent invasion, and chemotactic and proliferative responses to collagen type I. Our work indicates an essential role for DDR1 signaling in key prometastatic features of collagen type I in human carcinoma cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"69-81"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1733892","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37670746","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: 9
Platelet endothelial aggregation receptor-1 regulates bovine muscle satellite cell migration and differentiation via integrin beta-1 and focal adhesion kinase. 血小板内皮聚集受体-1通过整合素-1和局灶黏附激酶调控牛肌肉卫星细胞的迁移和分化。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619434
Yusheng Pang, Ziheng Zhang, Zhao Wang, Yuxin Wang, Yunqin Yan, Shufeng Li, Huili Tong
{"title":"Platelet endothelial aggregation receptor-1 regulates bovine muscle satellite cell migration and differentiation via integrin beta-1 and focal adhesion kinase.","authors":"Yusheng Pang,&nbsp;Ziheng Zhang,&nbsp;Zhao Wang,&nbsp;Yuxin Wang,&nbsp;Yunqin Yan,&nbsp;Shufeng Li,&nbsp;Huili Tong","doi":"10.1080/19336918.2019.1619434","DOIUrl":"https://doi.org/10.1080/19336918.2019.1619434","url":null,"abstract":"<p><p>PEAR1 is highly expressed at bovine MDSC differentiation. However, its biological function remains unclear. Western blotting results showed that PEAR1 increased between day 0 and day 2 of cell differentiation and decreased from day 3. Moreover, scratch test showed that wound healing rate increased after PEAR1 overexpression and decreased upon its suppression. Meanwhile, we found that, upon PEAR1 induction, both the expression of the focal adhesion-associated and MyoG, and the myotube fusion rate increased. However, when PEAR1 was suppressed, opposite results were obtained. Immunoprecipitation revealed an association between PEAR1 and ITGB1. Notably, inhibition of FAK and ITGB1 repressed cell differentiation. In conclusion, our study indicated that PEAR1 is involved in the regulation of bovine MDSC migration and differentiation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"192-202"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1619434","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37245494","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: 8
Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression. circ_0020397在颅内动脉瘤中的表达减少可能通过miR-138的表达增加和随后的KDR表达减少导致血管平滑肌细胞增殖减少。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619432
Yushe Wang, Yong Wang, Yu Li, Bin Wang, Zhuang Miao, Xianzhi Liu, Yuanyuan Ma
{"title":"Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression.","authors":"Yushe Wang,&nbsp;Yong Wang,&nbsp;Yu Li,&nbsp;Bin Wang,&nbsp;Zhuang Miao,&nbsp;Xianzhi Liu,&nbsp;Yuanyuan Ma","doi":"10.1080/19336918.2019.1619432","DOIUrl":"https://doi.org/10.1080/19336918.2019.1619432","url":null,"abstract":"<p><p>Dysfunction of vascular smooth muscle cells (VSMCs) mediates intracranial aneurysm (IA). KDR is reported to alleviate IA progression via promoting VSMC proliferation, while the upstream regulators are still unclear. Arterial wall tissues at the aneurysm site from 12 patients were obtained. The real-time PCR result indicated that circRNA_0020397 was down-regulated, but miR-138 was up-regulated in artery wall tissues and cells of IA. Overexpressed circRNA_0020397 promoted proliferation of human umbilical artery SMCs. MiR-138 negatively regulated KDR via binding with 3'UTR of KDR mRNA. The expression of circRNA_0020397 was negatively correlated with miR-138. In conclusion, our findings demonstrated that decreased expression of circRNA_0020397 in IA may contribute to the decreased VSMC proliferation via increasing miR-138 expression and subsequently decreasing KDR expression.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"220-228"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1619432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37421594","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: 27
BECN1 promotes the migration of NSCLC cells through regulating the ubiquitination of Vimentin. BECN1通过调控Vimentin泛素化促进NSCLC细胞的迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1638690
Zhujun Cheng, Hongbo Xin, Tianyu Han
{"title":"BECN1 promotes the migration of NSCLC cells through regulating the ubiquitination of Vimentin.","authors":"Zhujun Cheng,&nbsp;Hongbo Xin,&nbsp;Tianyu Han","doi":"10.1080/19336918.2019.1638690","DOIUrl":"https://doi.org/10.1080/19336918.2019.1638690","url":null,"abstract":"<p><p>BECN1/Beclin1 is one of the key proteins in autophagy regulation. However, the biological functions of BECN1 in non-small cell lung cancer (NSCLC) were obscure. Here, we found that neither BECN1 knockdown nor overexpression affected the proliferation of NSCLC cells. Surprisingly, BECN1 overexpression increased cell migration and knocking down BECN1 significantly reduced the migratory ability of NSCLC cells. We further demonstrated that BECN1 could interact with Vimentin and affected its K48-linked ubiquitination. What's more, BECN1 could also interact with ubiquitin-specific peptidase 14 (USP14), the key de-ubiquitinase of Vimentin, and regulated USP14 mediated de-ubiquitination of Vimentin. Thus, our studies revealed an oncosupportive role of BECN1 in the migration of NSCLC cells through regulating the ubiquitination of Vimentin.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"249-259"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1638690","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37397258","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: 15
Fluid shear stress induces cell migration and invasion via activating autophagy in HepG2 cells. 流体剪切应力通过激活HepG2细胞的自噬诱导细胞迁移和侵袭。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2019-01-31 DOI: 10.1080/19336918.2019.1568141
Zhiping Yan, Guanyue Su, Wenbo Gao, Jia He, Yang Shen, Ye Zeng, Xiaoheng Liu
{"title":"Fluid shear stress induces cell migration and invasion via activating autophagy in HepG2 cells.","authors":"Zhiping Yan,&nbsp;Guanyue Su,&nbsp;Wenbo Gao,&nbsp;Jia He,&nbsp;Yang Shen,&nbsp;Ye Zeng,&nbsp;Xiaoheng Liu","doi":"10.1080/19336918.2019.1568141","DOIUrl":"https://doi.org/10.1080/19336918.2019.1568141","url":null,"abstract":"<p><p>Fluid shear stress (FSS) regulates the metastasis of hepatocellular carcinoma (HCC). In the present study, we aimed to study the role of autophagy in HCC cells under FSS. The results showed that FSS upregulated the protein markers of autophagy, induced LC3B aggregation and formation of autophagosomes. Inhibition of integrin by Cliengitide (Cli) or inhibition of the microfilaments formation both inhibited the activation of autophagy in HepG2 under FSS. In addition, Cli inhibited the microfilaments formation and expressions of Rac1 and RhoA in HepG2 cells under FSS. Finally, inhibition of autophagy suppressed the cell migration and invasion in HepG2 under FSS. In conclusion, FSS induced autophagy to promote migration and invasion of HepG2 cells via integrin/cytoskeleton pathways.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"152-163"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1568141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36925651","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: 25
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