Ju LL, Chen L, Li JH, Wang YF, Lu RJ, Bian ZL, Shao JG. Effect of NDC80 in human hepatocellular carcinoma. World J Gastroenterol 2017; 23(20): 3675-3683 [PMID: 28611520 DOI: 10.3748/wjg.v23.i20.3675]
Corresponding Author of This Article
Zhao-Lian Bian, PhD, Nantong Institute of Liver Diseases, Nantong Third People’s Hospital, Nantong University, No. 60, Middle Qingnian Road, Nantong 226006, Jiangsu Province, China. bianzhaolian1998@163.com
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Basic Study
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Ju LL, Chen L, Li JH, Wang YF, Lu RJ, Bian ZL, Shao JG. Effect of NDC80 in human hepatocellular carcinoma. World J Gastroenterol 2017; 23(20): 3675-3683 [PMID: 28611520 DOI: 10.3748/wjg.v23.i20.3675]
Lin-Ling Ju, Lin Chen, Yi-Fan Wang, Ru-Jian Lu, Zhao-Lian Bian, Jian-Guo Shao, Nantong Institute of Liver Diseases, Nantong Third People’s Hospital, Nantong University, Nantong 226006, Jiangsu Province, China
Jun-Hong Li, Hematology Laboratory, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Author contributions: Ju LL, Chen L and Li JH contributed equally to this work; all authors made substantial contributions to the conception and design of the study and data acquisition and interpretation, and revised the manuscript and approved the final version to be published.
Supported byHealth 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; and Jiangsu Provincial Commission of Health and Family Planning, No. H201453.
Institutional review board statement: This study was reviewed and approved by the Institutional Review Board of Nantong Third People’s Hospital Affiliated to Nantong University, Nantong, China.
Informed consent statement: All tissue samples were taken from the patients after informed consent.
Conflict-of-interest statement: All authors declare that they have no competing interests related to this study.
Correspondence to: Zhao-Lian Bian, PhD, Nantong Institute of Liver Diseases, Nantong Third People’s Hospital, Nantong University, No. 60, Middle Qingnian Road, Nantong 226006, Jiangsu Province, China. bianzhaolian1998@163.com
Telephone: +86-139-62910367 Fax: +86-513-85512674
Received: December 1, 2016 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
Abstract
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.
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.
