Cell Adhesion & Migration最新文献

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TIMP-2 inhibits metastasis and predicts prognosis of colorectal cancer via regulating MMP-9. TIMP-2通过调控MMP-9抑制结直肠癌转移并预测预后。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1639303
Weimin Wang, Dan Li, Liangliang Xiang, Mengying Lv, Li Tao, Tengyang Ni, Jianliang Deng, Xiancheng Gu, Sunagawa Masatara, Yanqing Liu, Yan Zhou
{"title":"TIMP-2 inhibits metastasis and predicts prognosis of colorectal cancer via regulating MMP-9.","authors":"Weimin Wang,&nbsp;Dan Li,&nbsp;Liangliang Xiang,&nbsp;Mengying Lv,&nbsp;Li Tao,&nbsp;Tengyang Ni,&nbsp;Jianliang Deng,&nbsp;Xiancheng Gu,&nbsp;Sunagawa Masatara,&nbsp;Yanqing Liu,&nbsp;Yan Zhou","doi":"10.1080/19336918.2019.1639303","DOIUrl":"https://doi.org/10.1080/19336918.2019.1639303","url":null,"abstract":"<p><p>Colorectal cancer has a common cause of morbidity and mortality. Therefore, it is urgent to detect reliable biomarkers to predict prognosis in CRC. Here, we determined the expression of TIMP-2 and MMP-9 in a  CRC tissue microarray by immunohistochemistry. We found that lower TIMP-2 or/and higher MMP-9 expression in cancer tissues was correlated with poorer overall survival (OS). TIMP-2 or MMP-9 expression was independent prognostic factors for CRC. Furthermore, TIMP-2 and MMP-9 expression had a synergistic role as efficient prognostic indicators for CRC patients. In vitro and in vivo, TIMP-2 could inhibit HCT 116 cells invasion and migration by regulating MMP-9. In sum, a combined expression of TIMP-2 and MMP-9 as efficient prognostic indicators was found for the first time.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"273-284"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1639303","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37134835","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: 31
Recapitulation of molecular regulators of nuclear motion during cell migration. 细胞迁移过程中核运动的分子调节因子的综述。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-09-27 DOI: 10.1080/19336918.2018.1506654
Alexandra Sneider, Jungwon Hah, Denis Wirtz, Dong-Hwee Kim
{"title":"Recapitulation of molecular regulators of nuclear motion during cell migration.","authors":"Alexandra Sneider,&nbsp;Jungwon Hah,&nbsp;Denis Wirtz,&nbsp;Dong-Hwee Kim","doi":"10.1080/19336918.2018.1506654","DOIUrl":"10.1080/19336918.2018.1506654","url":null,"abstract":"<p><p>Cell migration is a highly orchestrated cellular event that involves physical interactions of diverse subcellular components. The nucleus as the largest and stiffest organelle in the cell not only maintains genetic functionality, but also actively changes its morphology and translocates through dynamic formation of nucleus-bound contractile stress fibers. Nuclear motion is an active and essential process for successful cell migration and nucleus self-repairs in response to compression and extension forces in complex cell microenvironment. This review recapitulates molecular regulators that are crucial for nuclear motility during cell migration and highlights recent advances in nuclear deformation-mediated rupture and repair processes in a migrating cell.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"50-62"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1506654","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36530139","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
Continuous, label-free, 96-well-based determination of cell migration using confluence measurement. 连续,无标记,96孔为基础的测定细胞迁移使用合流测量。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-10-08 DOI: 10.1080/19336918.2018.1526612
Christian Mayr, Marlena Beyreis, Heidemarie Dobias, Martin Gaisberger, Julia Fuchs, Martin Pichler, Markus Ritter, Martin Jakab, Katharina Helm, Daniel Neureiter, Tobias Kiesslich
{"title":"Continuous, label-free, 96-well-based determination of cell migration using confluence measurement.","authors":"Christian Mayr,&nbsp;Marlena Beyreis,&nbsp;Heidemarie Dobias,&nbsp;Martin Gaisberger,&nbsp;Julia Fuchs,&nbsp;Martin Pichler,&nbsp;Markus Ritter,&nbsp;Martin Jakab,&nbsp;Katharina Helm,&nbsp;Daniel Neureiter,&nbsp;Tobias Kiesslich","doi":"10.1080/19336918.2018.1526612","DOIUrl":"https://doi.org/10.1080/19336918.2018.1526612","url":null,"abstract":"<p><p>Cellular migration is essential in diverse physiological and pathophysiological processes. Here, we present a protocol for quantitative analysis of migration using confluence detection allowing continuous, non-endpoint measurement with minimal hands-on time under cell incubator conditions. Applicability was tested using substances which enhance (EGF) or inhibit (cytochalasin D, ouabain) migration. Using a gap-closure assay we demonstrate that automated confluence detection monitors cellular migration in the 96-well microplate format. Quantification by % confluence, % cell free-area or % confluence in cell-free area against time, allows detailed analysis of cellular migration. The study describes a practicable approach for continuous, non-endpoint measurement of migration in 96-well microplates and for detailed data analysis, which allows for medium/high-throughput analysis of cellular migration in vitro.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"76-82"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1526612","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36554311","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: 1
Stable contacts of naïve CD4 T cells with migratory dendritic cells are ICAM-1-dependent but dispensable for proliferation in vivo. naïve CD4 T细胞与迁移树突状细胞的稳定接触依赖于icam -1,但对于体内增殖是必不可少的
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1644857
Stav Kozlovski, Ofir Atrakchi, Sara W Feigelson, Ziv Shulman, Ronen Alon
{"title":"Stable contacts of naïve CD4 T cells with migratory dendritic cells are ICAM-1-dependent but dispensable for proliferation in vivo.","authors":"Stav Kozlovski, Ofir Atrakchi, Sara W Feigelson, Ziv Shulman, Ronen Alon","doi":"10.1080/19336918.2019.1644857","DOIUrl":"10.1080/19336918.2019.1644857","url":null,"abstract":"<p><p>It is unclear if naïve T cells require dendritic cell ICAMs to proliferate inside lymph nodes. To check if and when CD4 lymphocytes use ICAMs on migratory DCs, wild-type and ICAM-1 and 2 double knock out bone marrow-derived DCs pulsed with saturating levels of an OT-II transgene-specific ovalbumin-derived peptide were co-transferred into skin-draining lymph nodes. Intravital imaging of OT-II lymphocytes entering these lymph nodes revealed that ICAM-1 and -2 deficient migratory DCs formed fewer stable conjugates with OT-II lymphocytes but promoted normal T cell proliferation. DC ICAMs were also not required for unstable TCR-dependent lymphocyte arrests on antigen presenting migratory DCs. Thus, rare antigen-stimulated ICAM-stabilized T-DC conjugates are dispensable for CD4 lymphocyte proliferation inside lymph nodes.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"315-321"},"PeriodicalIF":3.3,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48937918","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: 0
Sirtuin 3 promotes microglia migration by upregulating CX3CR1. Sirtuin 3通过上调CX3CR1促进小胶质细胞迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1629224
Runjing Cao, Shiping Li, Junxiang Yin, Li Guo, Jiong Shi
{"title":"Sirtuin 3 promotes microglia migration by upregulating CX3CR1.","authors":"Runjing Cao,&nbsp;Shiping Li,&nbsp;Junxiang Yin,&nbsp;Li Guo,&nbsp;Jiong Shi","doi":"10.1080/19336918.2019.1629224","DOIUrl":"https://doi.org/10.1080/19336918.2019.1629224","url":null,"abstract":"<p><p>We studied the role of Sirtuin 3 (SIRT3) in microglial cell migration in ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of focal ischemia. We then applied lentivirus-packaged SIRT3 overexpression and knock down in microglial N9 cells to investigate the underlying mechanism driving microglial cell migration. More microglial cells appeared in the ischemic lesion side after MCAO. The levels of SIRT3 were increased in macrophages, the main source of microglia, after ischemia. CX3CR1 levels were increased with SIRT3 overexpression. SIRT3 promoted microglial N9 cells migration by upregulating CX3CR1 in both normal and glucose deprived culture media. These effects were G protein-dependent. Our study for the first time shows that SIRT3 promotes microglia migration by upregulating CX3CR1.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"229-235"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1629224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37336453","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
Caffeine inhibits hypoxia-induced renal fibroblast activation by antioxidant mechanism. 咖啡因通过抗氧化机制抑制缺氧诱导的肾成纤维细胞活化。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1638691
Angkhana Nilnumkhum, Rattiyaporn Kanlaya, Sunisa Yoodee, Visith Thongboonkerd
{"title":"Caffeine inhibits hypoxia-induced renal fibroblast activation by antioxidant mechanism.","authors":"Angkhana Nilnumkhum,&nbsp;Rattiyaporn Kanlaya,&nbsp;Sunisa Yoodee,&nbsp;Visith Thongboonkerd","doi":"10.1080/19336918.2019.1638691","DOIUrl":"https://doi.org/10.1080/19336918.2019.1638691","url":null,"abstract":"<p><p>Caffeine has been demonstrated to possess anti-fibrotic activity against liver fibrosis. However, its role in renal fibrosis remained unclear. This study investigated the effects of caffeine on renal fibroblast activation induced by hypoxia (one of the inducers for renal fibrosis). BHK-21 fibroblasts were cultured under normoxia or hypoxia with or without caffeine treatment. Hypoxia increased levels of fibronectin, α-smooth muscle actin, actin stress fibers, intracellular reactive oxygen species (ROS), and oxidized proteins. However, caffeine successfully preserved all these activated fibroblast markers to their basal levels. Cellular catalase activity was dropped under hypoxic condition but could be reactivated by caffeine. <i>Hif1a</i> gene and stress-responsive Nrf2 signaling molecule were elevated/activated by hypoxia, but only Nrf2 could be partially recovered by caffeine. These data suggest that caffeine exhibits anti-fibrotic effect against hypoxia-induced renal fibroblast activation through its antioxidant property to eliminate intracellular ROS, at least in part, via downstream catalase and Nrf2 mechanisms.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"260-272"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1638691","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37393611","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
Neutrophils as a source of branched-chain, aromatic and positively charged free amino acids. 中性粒细胞是支链、芳香和带正电的游离氨基酸的来源。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-10-29 DOI: 10.1080/19336918.2018.1540903
Svetlana I Galkina, Natalia V Fedorova, Alexander L Ksenofontov, Vladimir I Stadnichuk, Ludmila A Baratova, Galina F Sud'Ina
{"title":"Neutrophils as a source of branched-chain, aromatic and positively charged free amino acids.","authors":"Svetlana I Galkina,&nbsp;Natalia V Fedorova,&nbsp;Alexander L Ksenofontov,&nbsp;Vladimir I Stadnichuk,&nbsp;Ludmila A Baratova,&nbsp;Galina F Sud'Ina","doi":"10.1080/19336918.2018.1540903","DOIUrl":"https://doi.org/10.1080/19336918.2018.1540903","url":null,"abstract":"<p><p>Neutrophils release branched-chain (valine, isoleucine, leucine), aromatic (tyrosine, phenylalanine) and positively charged free amino acids (arginine, ornithine, lysine, hydroxylysine, histidine) when adhere and spread onto fibronectin. In the presence of agents that impair cell spreading or adhesion (cytochalasin D, fMLP, nonadhesive substrate), neutrophils release the same amino acids, except for a sharp decrease in hydroxylysine and an increase in phenylalanine, indicating their special connection with cell adhesion. Plasma of patients with diabetes is characterized by an increased content of branched-chain and aromatic amino acids and a reduced ratio of arginine/ornithine compared to healthy human plasma. Our data showed that the secretion of neutrophils, regardless of their adhesion state, can contribute to this shift in the amino acid content. Abbreviations: BCAAs: branched-chain amino acids; Е2: 17β-estradiol; LPS: lipopolysaccharide from Salmonella enterica serovar Typhimurium; fMLP: N-formylmethionyl-leucyl-phenylalanine.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"98-105"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1540903","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36605785","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
Small G protein signalling modulator 2 (SGSM2) is involved in oestrogen receptor-positive breast cancer metastasis through enhancement of migratory cell adhesion via interaction with E-cadherin. 小G蛋白信号调节因子2 (SGSM2)通过与E-cadherin相互作用增强迁移细胞粘附,参与雌激素受体阳性乳腺癌转移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2019-02-11 DOI: 10.1080/19336918.2019.1568139
Juo-Han Lin, Wen-Jui Lee, Han-Chung Wu, Chih-Hsiung Wu, Li-Ching Chen, Chi-Cheng Huang, Hang-Lung Chang, Tzu-Chun Cheng, Hui-Wen Chang, Chi-Tang Ho, Shih-Hsin Tu, Yuan-Soon Ho
{"title":"Small G protein signalling modulator 2 (SGSM2) is involved in oestrogen receptor-positive breast cancer metastasis through enhancement of migratory cell adhesion via interaction with E-cadherin.","authors":"Juo-Han Lin,&nbsp;Wen-Jui Lee,&nbsp;Han-Chung Wu,&nbsp;Chih-Hsiung Wu,&nbsp;Li-Ching Chen,&nbsp;Chi-Cheng Huang,&nbsp;Hang-Lung Chang,&nbsp;Tzu-Chun Cheng,&nbsp;Hui-Wen Chang,&nbsp;Chi-Tang Ho,&nbsp;Shih-Hsin Tu,&nbsp;Yuan-Soon Ho","doi":"10.1080/19336918.2019.1568139","DOIUrl":"https://doi.org/10.1080/19336918.2019.1568139","url":null,"abstract":"<p><p>The function of small G protein signalling modulators (SGSM1/2/3) in cancer remains unknown. Our findings demonstrated that SGSM2 is a plasma membrane protein that strongly interacted with E-cadherin/β-catenin. SGSM2 downregulation enhanced the phosphorylation of focal adhesion kinase (FAK; Y576/577), decreased the expression of epithelial markers such as E-cadherin, β-catenin, and Paxillin, and increased the expression of Snail and Twist-1, which reduced cell adhesion and promoted cancer cell migration. Oestrogen and fibronectin treatment was found to promote the colocalization of SGSM2 at the leading edge with phospho-FAK (Y397). The BioGRID database showed that SGSM2 potentially interacts with cytoskeleton remodelling and cell-cell junction proteins. These evidences suggest that SGSM2 plays a role in modulating cell adhesion and cytoskeleton dynamics during cancer migration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"120-137"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1568139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36545940","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
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
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