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Down-regulation of CMTM8 Induces Epithelial-to-Mesenchymal Transition-like Changes via c-MET/Extracellular Signal-regulated Kinase (ERK) Signaling
Zhang, Wenjuan2,3; Mendoza, Michelle C.1; Pei, Xiaolei2; Ilter, Didem1; Mahoney, Sarah J.1; Zhang, Yingmei2; Ma, Dalong2; Blenis, John1; Wang, Ying2
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2012-04-06
DOI10.1074/jbc.M111.258236
287期:15页:11850-11858
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]HEPATOCYTE GROWTH-FACTOR ; HUMAN HEPATOCELLULAR-CARCINOMA ; EARLY GENE-PRODUCTS ; COLORECTAL-CANCER ; POOR-PROGNOSIS ; PATHWAY ; EXPRESSION ; TRANSFORMATION ; PROGRESSION ; ACTIVATION
英文摘要

The acquisition of an invasive phenotype is a critical turning point for malignant tumor cells. CMTM8, a potential tumor suppressor, is frequently down-regulated in solid tumors, and its overexpression induces tumor cell apoptosis. Here, we identify a new role for CMTM8 in regulating tumor cell migration. Reducing CMTM8 expression in HepG2 hepatocellular carcinoma cells results in the acquisition of epithelial-to-mesenchymal transition (EMT) features, including a morphological change from organized epithelial sheets to scattered fibroblast-like shapes, reduction of the epithelial marker E-cadherin, and an increased invasive and migratory ability. These phenotypic changes are mediated in large part by the ERK-MAPK pathway, as the MEK inhibitor U0126 and shRNA-mediated knockdown of ERK2 significantly reversed these phenotypes. Hepatocyte growth factor binding to the c-MET receptor is known to induce EMT in HepG2 cells. We found that CMTM8 knockdown in HepG2 cells induced c-MET signaling and ERK activation. Inhibition of c-MET signaling with the small molecule inhibitor SU11274 or c-MET RNAi blocked the EMT-like changes following CMTM8 knockdown. CMTM8 overexpression in HepG2 cells inhibited hepatocyte growth factor-induced EMT-like morphological changes and cell motility. Down-regulation of CMTM8 also promoted an EMT-like change in MCF-10A cells, indicating a broader role for CMTM8 in regulating cellular transformation.

语种英语
WOS记录号WOS:000302782200024
项目编号R37CA46595 ; 81071749 ; 30872292 ; 90813025 ; 2012CB518000 ; 2009ZX09503-004
资助机构National Institutes of Health from NCI ; National Natural Science Foundation of China ; National Basic Research Program of China ; National Key New Drug Creation Program of China ; China Scholarship Council ; Susan G. Komen for the Cure
引用统计
被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54882
专题北京大学基础医学院
作者单位1.Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
2.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Key Lab Med Immunol,Minist Hlth,Dept Immunol, Beijing 100191, Peoples R China
3.Capital Med Univ, Peking Univ, Hosp 9, Beijing Shijitan Hosp,Canc Res Lab, Beijing 100038, Peoples R China
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GB/T 7714
Zhang, Wenjuan,Mendoza, Michelle C.,Pei, Xiaolei,et al. Down-regulation of CMTM8 Induces Epithelial-to-Mesenchymal Transition-like Changes via c-MET/Extracellular Signal-regulated Kinase (ERK) Signaling[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2012,287(15):11850-11858.
APA Zhang, Wenjuan.,Mendoza, Michelle C..,Pei, Xiaolei.,Ilter, Didem.,Mahoney, Sarah J..,...&Wang, Ying.(2012).Down-regulation of CMTM8 Induces Epithelial-to-Mesenchymal Transition-like Changes via c-MET/Extracellular Signal-regulated Kinase (ERK) Signaling.JOURNAL OF BIOLOGICAL CHEMISTRY,287(15),11850-11858.
MLA Zhang, Wenjuan,et al."Down-regulation of CMTM8 Induces Epithelial-to-Mesenchymal Transition-like Changes via c-MET/Extracellular Signal-regulated Kinase (ERK) Signaling".JOURNAL OF BIOLOGICAL CHEMISTRY 287.15(2012):11850-11858.
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