摘要
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. Over?expression 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.
Background： Hepatocellular carcinoma （HCC） is a common malignant tumor in the world, especially in China. As a member of the inhibitor of diferentiation （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. Over-expression 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.
基金
supported in part by grants from the National Key Program for Basic Research of China(973)(No.2015CB553905)
the National Natural Science Foundation of China(Nos.81272438,81472726,81301859)
the Key Discipline and Specialty Foundation of Shanghai Municipal Commission of Health and Family Planning,the National Key Sci-Tech Special Project of China(No.2013ZX10002–011)
the SKLORG Research Foundation(Nos.91-12-04,91-13-02,91-14-09)
