Chemosensitization of HepG2 cells by suppression of NF-κB/p65 gene transcription with specific-si RNA
Chemosensitization of HepG2 cells by suppression of NF-κB/p65 gene transcription with specific-si RNA作者机构：Research Center of Clinical Medicine Affiliated Hospital of Nantong University Department of Immunology Medical School of Nantong University Department of Oncology Affiliated Hospital of Nantong University
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2015年第21卷第45期
页 面：12814-12821页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：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 the international S&T Cooperation Program(2013DFA32150)of China
主 题：Hepatocellular carcinoma Nuclear factorκB Multidru
摘 要：AIM: To investigate small interfering RNA(si RNA)-mediated inhibition of nuclear factor-kappa B(NF-κB) activation and multidrug-resistant(MDR) phenotype formation in human Hep G2 cells. METHODS: Total RNA was extracted from human Hep G2 or LO2 cells. NF-κB/p65 m RNA was amplified by nested reverse transcription polymerase chain reaction and confirmed by sequencing. NF-κB/p65 was analyzed by immunohistochemistry. Specific-si RNA was transfected to Hep G2 cells to knock down NF-κB/p65 expression. The effects on cell proliferation, survival, and apoptosis were assessed, and the level of NF-κB/p65 or P-glycoprotein(P-gp) was quantitatively analyzed by enzyme-linked immunosorbent ***: Hep G2 cells express NF-κB/p65 and express relatively less phosphorylated p65(P-p65) and little P-gp. After treatment of Hep G2 cells with different doses of doxorubicin, the expression of NF-κB/p65, P-p65, and especially P-gp were dose-dependently upregulated. After Hep G2 cells were transfected with NF-κB/p65 si RNA(100 nmol/L), the expression of NF-κB/p65, P-p65, and P-gp were downregulatedsignificantly and dose-dependently. The viability of Hep G2 cells was decreased to 23% in the combination NF-κB/p65 si RNA(100 nmol/L) and doxorubicin(0.5 μmol/L) group and 47% in the doxorubicin(0.5 μmol/L) group(t = 7.043, P 0.001). CONCLUSION: Knockdown of NF-κB/p65 with si RNA is an effective strategy for inhibiting Hep G2 cell growth by downregulating P-gp expression associated chemosensitization and apoptosis induction.
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