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学科主题基础医学
CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation
Liu, Baocai1; Su, Yu1,2; Li, Ting1; Yuan, Wanqiong1; Mo, Xiaoning1; Li, Henan1,3; He, Qihua4; Ma, Dalong1; Han, Wenling1
关键词NSCLC CMTM7 EGFR AKT Rab5
刊名ONCOTARGET
2015-12-01
6期:38页:41092-41107
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Cell Biology
研究领域[WOS]Oncology ; Cell Biology
关键词[WOS]EPIDERMAL-GROWTH-FACTOR ; CHEMOKINE-LIKE FACTOR-1 ; FACTOR RECEPTOR ; TUMOR-SUPPRESSOR ; SMALL GTPASE ; ENDOCYTOSIS ; EXPRESSION ; TRAFFICKING ; TRANSDUCTION ; CHEMOTHERAPY
英文摘要

The dysregulation of epidermal growth factor receptor (EGFR) signaling has been well documented to contribute to the progression of non-small cell lung cancer (NSCLC), the leading cause of cancer death in the world. EGF-stimulated EGFR activation induces receptor internalization and degradation, which plays an important role in EGFR signaling. This process is frequently deregulated in cancer cells, leading to enhanced EGFR levels and signaling. Our previous study on CMTM7 is only limited to a brief description of the relationship of overexpressed CMTM7 with EGFR-AKT signaling. The biological functions of endogenous CMTM7 and its molecular mechanism remained unclear. In this study, we show that the stable knockdown of CMTM7 augments the malignant potential of NSCLC cells and enhances EGFR-AKT signaling by decreasing EGFR internalization and degradation. Mechanistically, CMTM7 knockdown reduces the activation of Rab5, a protein known to be required for early endosome fusion. In NSCLC, the loss of CMTM7 would therefore serve to sustain aberrant EGFR-mediated oncogenic signaling. Together, our findings highlight the role of CMTM7 in the regulation of EGFR signaling in tumor cells, revealing CMTM7 as a novel molecule related to Rab5 activation.

语种英语
WOS记录号WOS:000366115500054
项目编号81273207 ; 81201879
资助机构National Natural Science Foundation of China
引用统计
被引频次:6[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/50350
专题北京大学基础医学院_免疫学系
北京大学医学部管理机构_医学部
北京大学基础医学院
北京大学第二临床医学院_检验科
作者单位1.Peking Univ, Sch Basic Med Sci, Key Lab Med Immunol, Ctr Human Dis Genom,Dept Immunol, Beijing 100871, Peoples R China
2.Beijing Jishuitan Hosp, Dept Clin Lab, Beijing, Peoples R China
3.Peking Univ, Peoples Hosp, Dept Clin Lab, Beijing 100871, Peoples R China
4.Peking Univ, Med & Hlth Anal Ctr, Beijing 100871, Peoples R China
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GB/T 7714
Liu, Baocai,Su, Yu,Li, Ting,et al. CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation[J]. ONCOTARGET,2015,6(38):41092-41107.
APA Liu, Baocai.,Su, Yu.,Li, Ting.,Yuan, Wanqiong.,Mo, Xiaoning.,...&Han, Wenling.(2015).CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation.ONCOTARGET,6(38),41092-41107.
MLA Liu, Baocai,et al."CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation".ONCOTARGET 6.38(2015):41092-41107.
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