Open AccessId4 promotes cell proliferation in hepatocellular carcinoma
Author(s) -
Zhang Yang,
Zhang LiXing,
Liu XiaoQin,
Zhao FangYu,
Ge Chao,
Chen TaoYang,
Yao Ming,
Li JinJun
Publication year - 2017
Publication title -
cancer communications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.119
H-Index - 53
ISSN - 2523-3548
DOI - 10.1186/s40880-017-0186-7
Subject(s) - cell growth , gene knockdown , gene silencing , cancer research , hepatocellular carcinoma , cell , cell culture , biology , gene , biochemistry , genetics
Background Hepatocellular carcinoma (HCC) is a common malignant tumor in the world, especially in China. As a member of the inhibitor of differentiation ( Id ) family, Id4 has been reported to function in many cancer types, but relatively little is known about its role in HCC. The purpose of this study was to investigate the potential relationship between Id4 and HCC development and the underlying mechanism involving the function of Id4 in HCC. Methods We used quantitative real‐time polymerase chain reaction and Western blotting to examine the RNA and protein expression of Id4 . In addition, we used Cell Counting Kit‐8 assay and colony formation assay to identify the function of Id4 in the regulation of cell proliferation in human HCC. Results We found that the expression of Id4 protein was up‐regulated in tumor tissues from HCC patients. Overexpression of Id4 promoted HCC cell proliferation, clonogenicity in vitro, and tumorigenicity in vivo. Id4 knockdown experiments showed that silencing Id4 blocked the proliferation and colony formation ability of HCC cells in vitro. Furthermore, overexpression of CCAAT/enhancer‐binding protein β inhibited Id4 expression in HCC cells. Conclusion Id4 may be developed as a potent therapeutic agent for the treatment of HCC, but more details about the underlying mechanisms of action are needed.