Effects of NDUFA4 Overexpression on Growth of Human Colon Cancer Cells in vitro

Objective To investigate the effects of NDUFA4 overexpression on the growth of human colon cancer cells in vitro and to explore its potential mechanism. Methods The recombinant plasmid p-NDUFA4 (p-NDUFA4) and the control plasmid (p-Cont) were transiently transfected into human colon cancer HCT 116 c...

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Bibliographic Details
Main Authors: LIU Shiming, DING Tao, LEI Liangyu, HU Lin, MAO Ling, CHEN Chao, GUO Mengmeng, XU Lin
Format: Article
Language:zho
Published: Magazine House of Cancer Research on Prevention and Treatment 2019-05-01
Series:Zhongliu Fangzhi Yanjiu
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Online Access:http://html.rhhz.net/ZLFZYJ/html/8578.2019.18.1693.htm
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Summary:Objective To investigate the effects of NDUFA4 overexpression on the growth of human colon cancer cells in vitro and to explore its potential mechanism. Methods The recombinant plasmid p-NDUFA4 (p-NDUFA4) and the control plasmid (p-Cont) were transiently transfected into human colon cancer HCT 116 cells, respectively. Then, the relative expression level of NDUFA4 was determined by Real-time PCR and Western blot. The proliferation and colony formation ability of HCT116 cells were detected by CCK-8 assay and clone formation assay. The mRNA expression levels of cyclin-dependent kinase (CDK) 2, CDK3, CDK4 and CDK6 were determined by Real-time PCR. The expression levels of AKT (p-AKT) and ERK1/2(p-ERK1/2) were analyzed by Western blot. Results Compared with control group, the expression levels of NDUFA4 were increased remarkably in p-NDUFA4 group (all P < 0.01). The proliferation and clone formation capacity of HCT116 cells in p-NDUFA4 group were obviously increased (all P < 0.05). The expression of CDK2 and CDK3 mRNA were increased significantly(all P < 0.05). The expression of p-AKT and p-ERK1/2 were increased obviously (all P < 0.05). Conclusion The overexpression of NDUFA4 could significantly promote the growth of human colon cancer HCT116 cells in vitro, which might be closely related to the change of AKT and ERK signaling transduction.
ISSN:1000-8578
1000-8578