摘要
AIM To investigate the role of nuclear division cycle(NDC)80in human hepatocellular carcinogenesis.METHODS NDC80 gene expression was analyzed by real-time reverse transcription polymerase chain reaction in 47paired hepatocellular carcinoma(HCC)and adjacent tissues.The HCC cell line SMMC-7721 was transfected with lentivirus to silence endogenous NDC80 gene expression,which was confirmed by real-time polymerase chain reaction and western blotting.The effects of NDC80silencing on SMMC-7721 cell proliferation were evaluated by Cellomics Array Scan VTI imaging.Cell cycle analysis and apoptosis were detected with flow cytometry.Colony formation was assessed by fluorescence microscopy.RESULTS NDC80 expression levels in HCC tissues were significantly higher than those in the adjacent tissues.Functional studies demonstrated that NDC80 silencing significantly reduced SMMC-7721 cell proliferation and colony formation.Knockdown of NDC80 resulted in increased apoptosis and cell cycle arrest at S-phase.NDC80 contributed to HCC progression by reducing apoptosis and overcoming cell cycle arrest. CONCLUSION Elevated expression of NDC80 may play a role in promoting the development of HCC.
AIM To investigate the role of nuclear division cycle (NDC) 80 in human hepatocellular carcinogenesis. METHODS NDC80 gene expression was analyzed by real-time reverse transcription polymerase chain reaction in 47 paired hepatocellular carcinoma (HCC) and adjacent tissues. The HCC cell line SMMC-7721 was transfected with lentivirus to silence endogenous NDC80 gene expression, which was confirmed by real-time polymerase chain reaction and western blotting. The effects of NDC80 silencing on SMMC-7721 cell proliferation were evaluated by Cellomics ArrayScan VTI imaging. Cell cycle analysis and apoptosis were detected with flow cytometry. Colony formation was assessed by fluorescence microscopy. RESULTS NDC80 expression levels in HCC tissues were significantly higher than those in the adjacent tissues. Functional studies demonstrated that NDC80 silencing significantly reduced SMMC-7721 cell proliferation and colony formation. Knockdown of NDC80 resulted in increased apoptosis and cell cycle arrest at S-phase. NDC80 contributed to HCC progression by reducing apoptosis and overcoming cell cycle arrest. CONCLUSION Elevated expression of NDC80 may play a role in promoting the development of HCC.
基金
Health Bureau of Nantong City,No.WQ2016011
Nantong Science and Technology Bureau,No.MS22015105
National Natural Science Foundation of China,No.81601842
Science and Technology Development Project of Nantong City,China,No.HS2014061
Jiangsu Provincial Commission of Health and Family Planning,No.H201453
