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Cell Adhesion & Migration最新文献

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Interfering histone deacetylase 4 inhibits the proliferation of vascular smooth muscle cells via regulating MEG3/miR-125a-5p/IRF1. 干扰组蛋白去乙酰化酶4通过调节MEG3/miR-125a-5p/IRF1抑制血管平滑肌细胞增殖。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-08-29 DOI: 10.1080/19336918.2018.1506653
Xiangtao Zheng, Ziheng Wu, Ke Xu, Yihui Qiu, Xiang Su, Zhen Zhang, Mengtao Zhou
{"title":"Interfering histone deacetylase 4 inhibits the proliferation of vascular smooth muscle cells via regulating MEG3/miR-125a-5p/IRF1.","authors":"Xiangtao Zheng,&nbsp;Ziheng Wu,&nbsp;Ke Xu,&nbsp;Yihui Qiu,&nbsp;Xiang Su,&nbsp;Zhen Zhang,&nbsp;Mengtao Zhou","doi":"10.1080/19336918.2018.1506653","DOIUrl":"https://doi.org/10.1080/19336918.2018.1506653","url":null,"abstract":"<p><p>In this study, we investigated the role ofhistone deacetylase 4 (HDAC4) and MEG3/miR-125a-5p/interferonregulatoryfactor 1 (IRF1) on vascular smooth muscle cell (VSMCs)proliferation. Platelet derived growth factor (PDGF)-BB was used toinduce the proliferation and migration of VSMCs. The expressionsof MEG3, miR-125a-5p, HDAC4 and IRF1in VSMCs were detectedby qRT-PCR and western blot, respectively. ChIP assay was usedto determine the relationship between MEG3 and HDAC4. Doubleluciferase reporter assay was used to test the regulation betweenmiR-125-5p and IRF1. Results showed that PDGF-BB decreasedthe expression of MEG3 and IRF1, while increased the expressionof miR-125a-5p and HDAC4. In addition, HDAC4 knockdowninhibited the proliferation and migration of VSMCs via upregulatingMEG3 and downregulating miR-125a-5p. MiR-125a-5p inhibitorcould repress the proliferation and migration of VSMCs andalleviate intimal hyperplasia (IH) by directly upregulating IRF1expression. These results suggested that HDAC4 interferenceinhibited PDGF-BB-induced VSMCs proliferation via regulatingMEG3/miR-125a-5p/IRF1 axis, and then alleviated IH.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"41-49"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1506653","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36441031","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: 19
Downregulation of miR-200c stabilizes XIAP mRNA and contributes to invasion and lung metastasis of bladder cancer. miR-200c下调可稳定XIAP mRNA，参与膀胱癌的侵袭和肺转移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1633851
Honglei Jin, Lei Xue, Lan Mo, Dongyun Zhang, Xirui Guo, Jiheng Xu, Jingxia Li, Minggang Peng, Xuewei Zhao, Minghao Zhong, Dazhong Xu, Xue-Ru Wu, Haishan Huang, Chuanshu Huang
{"title":"Downregulation of miR-200c stabilizes XIAP mRNA and contributes to invasion and lung metastasis of bladder cancer.","authors":"Honglei Jin,&nbsp;Lei Xue,&nbsp;Lan Mo,&nbsp;Dongyun Zhang,&nbsp;Xirui Guo,&nbsp;Jiheng Xu,&nbsp;Jingxia Li,&nbsp;Minggang Peng,&nbsp;Xuewei Zhao,&nbsp;Minghao Zhong,&nbsp;Dazhong Xu,&nbsp;Xue-Ru Wu,&nbsp;Haishan Huang,&nbsp;Chuanshu Huang","doi":"10.1080/19336918.2019.1633851","DOIUrl":"https://doi.org/10.1080/19336918.2019.1633851","url":null,"abstract":"<p><p>Our previous studies have demonstrated that XIAP promotes bladder cancer metastasis through upregulating RhoGDIβ/MMP-2 pathway. However, the molecular mechanisms leading to the XIAP upregulation was unclear. In current studies, we found that XIAP was overexpressed in human high grade BCs, high metastatic human BCs, and in mouse invasive BCs. Mechanistic studies indicated that XIAP overexpression in the highly metastatic T24T cells was due to increased mRNA stability of XIAP that was mediated by downregulated miR-200c. Moreover, the downregulated miR-200c was due to CREB inactivation, while miR-200c downregulation reduced its binding to the 3'-UTR region of XIAP mRNA. Collectively, our results demonstrate the molecular basis leading to XIAP overexpression and its crucial role in BC invasion.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"236-248"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1633851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37363433","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
Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton. 槲皮素通过抑制iNOS/FAK/paxillin通路和调节细胞骨架抑制lps诱导的巨噬细胞迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-08-01 DOI: 10.1080/19336918.2018.1486142
Shuna Cui, Qingqing Wu, Juan Wang, Min Li, Jing Qian, Shihua Li
{"title":"Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton.","authors":"Shuna Cui,&nbsp;Qingqing Wu,&nbsp;Juan Wang,&nbsp;Min Li,&nbsp;Jing Qian,&nbsp;Shihua Li","doi":"10.1080/19336918.2018.1486142","DOIUrl":"https://doi.org/10.1080/19336918.2018.1486142","url":null,"abstract":"ABSTRACT The natural flavonoid quercetin has antioxidant, anti-inflammatory, and anticancer effects. We investigated the effect of quercetin on lipopolysaccharide (LPS)-induced macrophage migration. Quercetin significantly attenuated LPS-induced inducible nitric oxide synthase (iNOS)-derived nitric oxide (NO) production in RAW264.7 cells without affecting their viability. Additionally, quercetin altered the cell size and induced an elongated morphology and enlarged the vacuoles and concentrated nuclei. Quercetin significantly disrupted the F-actin cytoskeleton structure. Furthermore, quercetin strongly inhibited LPS-induced macrophage adhesion and migration in a dose-dependent manner. Moreover, quercetin inhibited the LPS-induced expression of p-FAK, p-paxillin, FAK, and paxillin as well as the cytoskeletal adapter proteins vinculin and Tensin-2. Therefore, quercetin suppresses LPS-induced migration by inhibiting NO production, disrupting the F-actin cytoskeleton, and suppressing the FAK–paxillin pathway. Quercetin may thus have potential as a therapeutic agent for chronic inflammatory diseases.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"1-12"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1486142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36260571","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: 49
Role of glycosylation in hypoxia-driven cell migration and invasion. 糖基化在缺氧驱动的细胞迁移和侵袭中的作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-08-19 DOI: 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,&nbsp;Patricio Silva,&nbsp;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}
引用次数: 17
The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells. 通过非典型蛋白激酶c激活的Cofilin调节肌动蛋白动力学调节结直肠癌细胞的转移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-11-18 DOI: 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,&nbsp;Rekha Patel,&nbsp;Raja Reddy Bommareddy,&nbsp;Khandker Mohammad Khalid,&nbsp;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}
引用次数: 14
T lymphocytes migrate upstream after completing the leukocyte adhesion cascade. T淋巴细胞完成白细胞粘附级联后向上游迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2019-03-17 DOI: 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,&nbsp;Alexander Buffone,&nbsp;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}
引用次数: 17
Protein kinase C Inhibitors selectively modulate dynamics of cell adhesion molecules and cell death in human colon cancer cells. 蛋白激酶C抑制剂选择性调节人结肠癌细胞粘附分子动力学和细胞死亡。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-10-11 DOI: 10.1080/19336918.2018.1530933
Muzaffer Dükel, Zehra Tavsan, Duygu Erdogan, Deniz Erkan Gök, Hulya Ayar Kayali
{"title":"Protein kinase C Inhibitors selectively modulate dynamics of cell adhesion molecules and cell death in human colon cancer cells.","authors":"Muzaffer Dükel,&nbsp;Zehra Tavsan,&nbsp;Duygu Erdogan,&nbsp;Deniz Erkan Gök,&nbsp;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}
引用次数: 8
The effect of cytokines produced by human adipose tissue on monocyte adhesion to the endothelium 人脂肪组织产生的细胞因子对单核细胞粘附内皮的影响
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-01-01 DOI: 10.1080/19336918.2019.1644856
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}
引用次数: 9
Splicing factor-modulated generation of mechano growth factor regulates physiological processes in osteoblasts under mechanical stimuli 剪接因子调节机械生长因子的产生调节成骨细胞在机械刺激下的生理过程
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-01-01 DOI: 10.1080/19336918.2019.1686103
Qian Yi, Huan Liu, Jianguo Feng, Yanjiao Wu, Weichao Sun, Mengting Ou, Liling Tang
{"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}
引用次数: 4
Paracrine signalling of AGR2 stimulates RhoA function in fibroblasts and modulates cell elongation and migration AGR2的旁分泌信号传导刺激成纤维细胞中的RhoA功能并调节细胞延伸和迁移
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-01-01 DOI: 10.1080/19336918.2019.1685928
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}
引用次数: 4
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