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Knockdown of PSMC3IP suppresses the proliferation and xenografted tumorigenesis of hepatocellular carcinoma cell
Author(s) -
Ding Jingli,
Li Yang,
Fan Huxiong,
Xu Weichang,
Gao Rifeng,
Bai Shuheng,
Zhu Zhigang,
Yang Wei,
Gong Yi,
Yang Juesheng,
Zhou Jianliang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27824
Subject(s) - gene knockdown , hepatocellular carcinoma , cancer research , carcinogenesis , cell growth , cell , chemistry , biology , apoptosis , medicine , cancer , genetics
Hepatocellular carcinoma (HCC) is the fifth most frequent malignancy and the second leading cause of cancer‐related death worldwide. Proteasome 26S subunit ATPase 3 interacting protein (PSMC3IP) is an oncogene in breast cancer, while its role in HCC remains unclear. Here, we found that PSMC3IP was critical for the cell proliferation and tumorigenic capacity of HCC cells. Upregulation of PSMC3IP was observed in HCC specimens, and high PSMC3IP expression predicted poor overall survival of HCC patients. In vitro, knockdown of PSMC3IP blunted the proliferation and colony formation of BEL‐7404 and SMMC‐7721 cells. Likewise, PSMC3IP silencing suppressed the xenografted tumor development of BEL‐7404 cells. Mechanistically, apoptosis was enhanced after PSMC3IP knockdown in both BEL‐7404 and SMMC‐7721 cells. At the molecular level, TP53 and GNG4 were upregulated and eukaryotic translation initiation factor 4E (EIF4E) and insulin like growth factor 1 receptor (IGF1R) were downregulated in shPSMC3IP compared with shCtrl BEL‐7404 cells. Therefore, targeting PSMC3IP maybe a promising strategy for HCC.