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FGFR1 regulates proliferation and metastasis by targeting CCND1 in FGFR1 amplified lung cancer. FGFR1在FGFR1扩增的肺癌中通过靶向CCND1调控增殖和转移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1766308
Ying Yang, Tingting Lu, Ziming Li, Shun Lu
{"title":"FGFR1 regulates proliferation and metastasis by targeting CCND1 in FGFR1 amplified lung cancer.","authors":"Ying Yang,&nbsp;Tingting Lu,&nbsp;Ziming Li,&nbsp;Shun Lu","doi":"10.1080/19336918.2020.1766308","DOIUrl":"https://doi.org/10.1080/19336918.2020.1766308","url":null,"abstract":"<p><p><b>Aims</b>: The analysis of the online databases revealed that CCND1 expression is correlated with poor prognosis in LSCC. We aimed to explore the function of CCND1 in tumor progression in LSCC.<b>Main methods</b>: The expression of mRNA was measured using qRT-PCR. Protein expression was assessed by Western blot. Cell migration and invasion were assessed by transwell assay.<b>Key findings</b>: CCND1 was co-overexpressed with FGFR1 in lung cancer patients. Overexpression of CCND1 promoted LSCC cell proliferation and metastasis. FGFR1 promoted the processes of EMT through AKT/MAPK signaling by targeting CCND1 in FGFR1-amplification cell lines.<b>Significance</b>: IIn conclusion, our study demonstrated the regulatory mechanism between CCND1 and FGFR1 in FGFR1 amplified LSCC. Co-targeting CCND1 and FGFR1 could provide greater clinical benefits.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"82-95"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1766308","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37912619","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: 23
Amblyomin-X, a recombinant Kunitz-type inhibitor, regulates cell adhesion and migration of human tumor cells. Amblyomin-X是一种重组kunitz型抑制剂，可调节人肿瘤细胞的粘附和迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 Epub Date: 2018-09-25 DOI: 10.1080/19336918.2018.1516982
Mariana Costa Braga Schmidt, Katia L P Morais, Maíra Estanislau Soares de Almeida, Asif Iqbal, Mauricio Barbugiani Goldfeder, Ana Marisa Chudzinski-Tavassi
{"title":"Amblyomin-X, a recombinant Kunitz-type inhibitor, regulates cell adhesion and migration of human tumor cells.","authors":"Mariana Costa Braga Schmidt,&nbsp;Katia L P Morais,&nbsp;Maíra Estanislau Soares de Almeida,&nbsp;Asif Iqbal,&nbsp;Mauricio Barbugiani Goldfeder,&nbsp;Ana Marisa Chudzinski-Tavassi","doi":"10.1080/19336918.2018.1516982","DOIUrl":"https://doi.org/10.1080/19336918.2018.1516982","url":null,"abstract":"<p><p>In a tumor microenvironment, endothelial cell migration and angiogenesis allow cancer to spread to other organs causing metastasis.  Indeed, a number of molecules that are involved in cytoskeleton re-organization and intracellular signaling have been investigated for their effects on tumor cell growth and metastasis. Alongside that, Amblyomin-X, a recombinant Kunitz-type protein, has been shown to reduce metastasis and tumor growth in in vivo experiments. In the present report, we provide a mechanistic insight to these antitumor effects, this is,  Amblyomin-X modulates Rho-GTPases and uPAR signaling, and reduces the release of MMPs, leading to disruption of the actin cytoskeleton and decreased cell migration of tumor cell lines. Altogether, our data support a role for Amblyomin-X as a novel potential antitumor drug.</p><p><strong>Abbreviations: </strong>Amb-X: Amblyomin-X; ECGF: endotelial cell growth factor; ECM: extracellular matrix; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HUVEC: human umbilical vein endothelial cell; LRP1: low-density lipoprotein receptor-related protein; MMP: matrix metalloproteinase; HPI-4: hedgehog pathway inhibitor 4; PAI-1: plasminogen activator inhibitor 1; PMA: phorbol 12-myristate-13-acetate; TFPI: tissue factor pathway inhibitor; uPA: urokinase plasminogen activator; uPAR: uPA receptor.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"129-138"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1516982","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36509658","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: 11
Fibronectin type III domain-containing 4 promotes the migration and differentiation of bovine skeletal muscle-derived satellite cells via focal adhesion kinase. 含纤维连接蛋白III型结构域4通过黏附激酶促进牛骨骼肌源卫星细胞的迁移和分化。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1810508
Zhao Wang, Zhiqi Wang, Yusheng Pang, Huili Tong, Yunqin Yan, Shuang Li, Shufeng Li
{"title":"Fibronectin type III domain-containing 4 promotes the migration and differentiation of bovine skeletal muscle-derived satellite cells via focal adhesion kinase.","authors":"Zhao Wang,&nbsp;Zhiqi Wang,&nbsp;Yusheng Pang,&nbsp;Huili Tong,&nbsp;Yunqin Yan,&nbsp;Shuang Li,&nbsp;Shufeng Li","doi":"10.1080/19336918.2020.1810508","DOIUrl":"https://doi.org/10.1080/19336918.2020.1810508","url":null,"abstract":"<p><p>FNDC4 is an anti-inflammatory factor that alters the activation state of macrophages; it is used to treat colitis in mice. However, its role in muscle formation and mechanism of function remains unknown. We found that FNDC4 promotes the bovine MDSCs migration and differentiation. Furthermore, we reported that it interacts with integrin β1 (ITGβ1). FAK, mediated by ITGβ1, regulates cell migration. Our results found FNDC4 to influence the expression of p-FAK, p-paxillin, and vinculin. Then, overexpressed or added FNDC4 protein could not influence migration and differentiation any more when the activated form of FAK was reduced. Therefore, we concluded that FNDC4 promotes the differentiation and migration of bovine MDSCs via the FAK, mediated by the ITGβ1 receptor.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"153-164"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1810508","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38340662","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
Hypoxia regulates human mast cell adhesion to fibronectin via the PI3K/AKT signaling pathway. 缺氧通过PI3K/AKT信号通路调节人肥大细胞对纤维连接蛋白的粘附。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2020-12-01 DOI: 10.1080/19336918.2020.1764690
Joanna Pastwińska, Aurelia Walczak-Drzewiecka, Magdalena Łukasiak, Marcin Ratajewski, Jarosław Dastych
{"title":"Hypoxia regulates human mast cell adhesion to fibronectin via the PI3K/AKT signaling pathway.","authors":"Joanna Pastwińska,&nbsp;Aurelia Walczak-Drzewiecka,&nbsp;Magdalena Łukasiak,&nbsp;Marcin Ratajewski,&nbsp;Jarosław Dastych","doi":"10.1080/19336918.2020.1764690","DOIUrl":"https://doi.org/10.1080/19336918.2020.1764690","url":null,"abstract":"<p><p>A decrease in oxygen concentration is a hallmark of inflammatory reactions resulting from infection or homeostasis disorders. Mast cells interact with extracellular matrix and other cells by adhesion receptors. We investigated the effect of hypoxia on integrin-mediated mast cell adhesion to fibronectin. We found that it was mediated by the α5/β1 receptor and that hypoxia significantly upregulated this process. Hypoxia-mediated increases in mast cell adhesion occurred without increased surface expression of integrins, suggesting regulation by inside-out integrin signaling. Hypoxia also mediated an increase in phosphorylation of Akt, and PI3'kinase inhibitors abolished hypoxia-mediated mast cell adhesion. Hypoxia upregulates the function of integrin receptors by PI3' kinase-dependent signaling. This process might be important for the location of mast cells at inflammatory sites.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"14 1","pages":"106-117"},"PeriodicalIF":3.2,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2020.1764690","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37952713","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: 3
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
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