JOURNAL OF PRACTICAL HEPATOLOGY ›› 2016, Vol. 19 ›› Issue (6): 704-708.doi: 10.3969/j.issn.1672-5069.2016.06.016

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Expression of IGF-1R/NF-kappa B and multi-drug resistance in insulin resistance-HepG2 and HepG2.2.15 cells in vitro

Wang Yilang,Yin Dian,Yang Li,et al.   

  1. Department of Oncology,Research Center of Clinical Medicine,First People’s Hospital Affiliated to Nantong University,Nantong,226001,Jiangsu Province,China
  • Received:2016-06-20 Online:2016-11-10 Published:2016-11-28
  • Contact: Yao Dengfu,E-mail:yaodf @ahnmc.com

Abstract: Objective To investigate the expression of insulin-like growth factor 1 receptor(IGF-1R),nuclear factor-κB(NF-κB) and the mechanism of multi-drug resistance(MDR) in insulin resistance(IR)- hepatoma cells in vitro. Methods The human hepatoma cells(HepG2 and HepG2.2.15) were induced by high concentration of insulin to establish a insulin resistance model. The expression of insulin receptor (InsR),IGF-1R,NF kappa B,P glycoprotein(P-gp) were detected by Western bloting and the effect of adriamycin on cell apoptosis were detected by flow cytometry(annexin V-FITC). Results IR model of hepatoma cells were established successfully by subjecting the HepG2 and HepG2.2.15 cells to 100 nmol/L and 1 000 n mol/L insulin respectively for 48 hours. The expression of IGF-1R,NF-kappa B and P-gp were up-regulated in IR hepatoma cells,while the InsR expression was down-regulated;After treatment of the two cells with 25 μg/ml doxorubicin for 24 hours,the apoptosis rate of IR-HpeG 2 cells (31.1% ±1.9%) was significantly lower than HepG2 cells [(49.7±2.2)%,P<0.01],and the apoptosis rate of IR-HepG2.2.15 cells(20.1±1.7)% was significantly lower than HepG2.2.15 cells[(33.8±1.8)%,P<0.01];The apoptotic rates of HepG2.2.15 or IR-HepG2.2.15 cells were significantly lower than HepG2 or IR-HepG2 cells(P<0.01),respectively. Conclusion The expression of IGF-1R, NF-kappa B and P-gp are up-regulated in IR-hepatoma cells,which might induce the MDR to adriamycin.

Key words: HepG2 cells, Insulin resistance, Insulin-like growth factor I receptor, NF-kappa B, P-glycoprotein, Multi-drug resistance