ISSN: 0973-7510

E-ISSN: 2581-690X

Wang Li, Yao Min, Yan Meijuan, Gu Xing, Yan Xiaodi and Yao Dengfu
1Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
J Pure Appl Microbiol. 2013;7(Spl. Edn.: April):461-467
© The Author(s). 2013
Received: 03/03/2013 | Accepted: 14/04/2013 | Published: 30/04/2013
Abstract

Hypoxia-inducible factor (HIF)-1a is a key transcription regulator for multiple angiogenic factors and appealing target and HIF-1a promotes angiogenesis are not fully understood. Therefore, we investigated the effects of silencing HIF-1a on proliferation of HepG2 cells and angiogenesis. After the cells transfected with HIF-1a miRNA at 72 h, HIF-1a expression was down to 23 % at mRNA level by quantitative real time PCR and 44 % at protein level by Western blotting. The expressions of the down-stream vascular endothelial growth factor and angiopoietin-2 were decreased 54 % and 34 % by enzyme-linked immunosorbent assay, respectively. The alteration of cell cycle proportion was 61.49 % in G1 phase, 22.40 % in S phase, and not in G2/M phase. The apoptotic ratio of HepG2 cells increased from 22.46 % to 36.99 % with 65.68 % of G1 phase and 19.47 % of S phase when HIF-1a activation interfering with miRNA plus doxorubicin by flow cytometry or annexin Annexin-V-FLUOS assay. The down-regulated HIF-1a expression resulted in decreasing angiogenic factors, inhibition of HepG2 cell growth, and inducing apoptosis. Therefore, we conclude that HIF-1a may serve as a useful molecular target for miRNA-based liver cancer therapy.

Keywords

HCC, HIF-1α, Ang-2, SiRNA, VEGF, Real-time PCR, Gene silencing

Article Metrics

Article View: 0

Share This Article

© The Author(s) 2013. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License which permits unrestricted use, sharing, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.