COMMD7 is correlated with a novel NF-κB positive feedback loop in hepatocellular carcinoma
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Lu Zheng1, Chang-Lin Deng1, Liang Wang1, Xiao-Bing Huang1, Nan You1, Yi-Chen Tang1, Ke Wu1, Ping Liang1, Na Mi1, Jing Li1
1Department of Hepatobiliary Surgery, Xinqiao Hospital of Third Military Medical University, Chongqing, 400037, China
Jing Li, email: [email protected]
Keywords: COMMD7, nuclear factor-kappa B, proliferation, apoptosis, hepatocellular carcinoma
Received: October 20, 2015 Accepted: March 31, 2016 Published: April 27, 2016
The correlation between nuclear factor-kappa B (NF-κB) and COMMD7 in hepatocellular carcinoma (HCC) development remained unclear. Here, our clinicopathological data showed that COMMD7 is overexpressed in HCC with a correlation to NF-κB. Using HepG2 and SMMC-7721 cells that aberrantly overexpressed COMMD7, we found that NF-κB directly binds with COMMD7 promoter and serves as an activator for COMMD7 transcription by luciferase reporter assay, chromatin immunoprecipitation (ChIP), and electrophoretic mobility shift assay (EMSA). In both HepG2 cells and SMMC-7721 cells, the silencing of COMMD7 significantly inhibited the cell proliferation, whereas NF-κB silencing inhibited the expression of COMMD7 and further inhibited cell proliferation. In addition, cell apoptosis was promoted by COMMD7 silencing, and further promoted by NF-κB silencing. Cell migration and invasion were also inhibited by COMMD7 silencing, and further inhibited by NF-κB silencing. Thus, COMMD7 is correlated with a novel NF-κB positive feedback loop in hepatocellular carcinoma. Developing strategies for the treatment of HCC should consider the correlation between NF-κB and COMMD7, so as to improve the specificity and sensitivity of therapy and to reduce toxicity.
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