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Id4 promotes cell proliferation in hepatocellular carcinoma

Overview of attention for article published in Cancer Communications, February 2017
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Title
Id4 promotes cell proliferation in hepatocellular carcinoma
Published in
Cancer Communications, February 2017
DOI 10.1186/s40880-017-0186-7
Pubmed ID
Authors

Yang Zhang, Li-Xing Zhang, Xiao-Qin Liu, Fang-Yu Zhao, Chao Ge, Tao-Yang Chen, Ming Yao, Jin-Jun Li

Abstract

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. 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. 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. 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.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 8 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 8 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 3 38%
Student > Ph. D. Student 1 13%
Professor > Associate Professor 1 13%
Lecturer 1 13%
Unknown 2 25%
Readers by discipline Count As %
Medicine and Dentistry 2 25%
Biochemistry, Genetics and Molecular Biology 1 13%
Immunology and Microbiology 1 13%
Nursing and Health Professions 1 13%
Unknown 3 38%