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©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 7, 2015; 21(45): 12814-12821
Published online Dec 7, 2015. doi: 10.3748/wjg.v21.i45.12814
Published online Dec 7, 2015. doi: 10.3748/wjg.v21.i45.12814
Chemosensitization of HepG2 cells by suppression of NF-κB/p65 gene transcription with specific-siRNA
Yun Shi, Si-Ye Wang, Min Yao, Wen-Li Sai, Wei Wu, Jun-Ling Yang, Wen-Jie Zheng, Deng-Fu Yao, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Min Yao, Department of Immunology, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China
Yin Cai, Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Author contributions: Shi Y, Wang SY, and Yao M contributed equally to this work, designed the research, analyzed the data, and wrote the first draft; Sai WL, Wu W, and Qiu LW performed quantitative real time PCR; Yang JL and Cai Y analyzed the data by Western blotting and ELISA; Zhang HJ and Zheng WJ performed immunohistochemistry, transfection, and cell proliferation, survival, and apoptosis assays; Yao DF is the guarantor and contributed to the design and interpretation of the study.
Supported by Grants from the Jiangsu Provincial Special Programs of Medical Science, BL2012053, HK201102; the Nantong Undertaking and Technological Innovation, HS2013007, BK2013048 and HS2014078; the Priority Academic Program Development of Higher Education Institution of Jiangsu Province, the National Natural Science Foundation, No. 81200634; and the international S &T Cooperation Program (2013DFA32150) of China.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Deng-Fu Yao, MD, PhD, Professor, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Telephone: +86-513-85052297 Fax: +86-513-85052523
Received: March 28, 2015
Peer-review started: March 29, 2015
First decision: April 24, 2015
Revised: July 4, 2015
Accepted: September 15, 2015
Article in press: September 15, 2015
Published online: December 7, 2015
Processing time: 252 Days and 21.3 Hours
Peer-review started: March 29, 2015
First decision: April 24, 2015
Revised: July 4, 2015
Accepted: September 15, 2015
Article in press: September 15, 2015
Published online: December 7, 2015
Processing time: 252 Days and 21.3 Hours
Core Tip
Core tip: Hepatic nuclear factor-kappa B (NF-κB) signaling pathway could be a potential target for designing highly effective therapeutic agents for the chemoprevention of hepatocellular carcinoma (HCC). Specific siRNAs used in combination with doxorubicin could enhance doxorubicin cytotoxicity in human HepG2 cells by downregulating NF-κB and P-glycoprotein expression. Stable NF-κB inhibition and chemosensitization could significantly inhibit tumor cell proliferation. Thus, the modulation of NF-κB might represent an advance in HCC therapy efficacy and is worthy of further research and investigation.