Published online May 28, 2017. doi: 10.3748/wjg.v23.i20.3675
Peer-review started: December 6, 2016
First decision: February 9, 2017
Revised: February 23, 2017
Accepted: March 20, 2017
Article in press: March 20, 2017
Published online: May 28, 2017
Processing time: 176 Days and 7 Hours
To investigate the role of nuclear division cycle (NDC)80 in human hepatocellular carcinogenesis.
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.
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.
Elevated expression of NDC80 may play a role in promoting the development of HCC.
Core tip: Nuclear division cycle (NDC)80 is a member of the NDC80 kinetochore complex and is highly expressed in cancer. NDC80 is a newly identified gene that is overexpressed in hepatocellular carcinoma (HCC). We analyzed the biological function of NDC80 in the proliferation and apoptosis of HCC cells, and provided new reference data and experimental support for HCC-targeting gene therapy.