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学科主题: 基础医学
题名:
CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation
作者: 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
发表日期: 2015-12-01
卷: 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
所属项目编号: 81273207 ; 81201879
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000366115500054
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50350
Appears in Collections:基础医学院_免疫学系_期刊论文

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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

Recommended Citation:
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.
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