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目的探讨IGF-ⅠR信号通路在西妥昔单抗抗HepG2细胞增殖中的作用。方法选用浓度递增的西妥昔单抗(5～500)mg/mL、胰岛素样生长因子(IGF)(2.5～250)μmol/L及其抑制剂aIR3(2.5～250)μmol/L,单独或联合作用于HepG2细胞,观察IGF与aIR3对西妥昔单抗抗HepG2增殖的影响。结果细胞培养72 h后,单药西妥昔单抗对HepG2细胞增殖的抑制作用呈浓度依赖性,西妥昔单抗联合aIR3组增殖抑制率在相应浓度下均显著高于同浓度的西妥昔单抗组(均为P<0.01),IGF(10～250)μmol/L与西妥昔单抗(20～500)mg/mL联合组增殖抑制率均显著低于相应浓度的西妥昔单抗组(均为P<0.01)。结论 IGF-ⅠR通路可影响西妥昔单抗抗HepG2细胞增殖的作用,可能是肝癌细胞株对西妥昔单抗耐药的机制之一。
Objective To investigate the role of IGF-ⅠR signaling pathway in the proliferation of cetuximab-resistant HepG2 cells. Methods The concentration of cetuximab (5 ~ 500) mg / mL, insulin-like growth factor (IGF) (2.5-250) μmol / L and its inhibitor aIR3 (2.5-250 μmol / Combined effect on HepG2 cells, observed IGF and aIR3 cetuximab anti-HepG2 proliferation. Results After 72 h of cell culture, the inhibitory effect of monotherapy cetuximab on HepG2 cell proliferation was concentration dependent. The inhibition rate of cetuximab plus aIR3 group was significantly higher than that of cetuxaban at the same concentration (All P <0.01). The inhibitory rates of proliferation in the combination of IGF (10 ~ 250) μmol / L and cetuximab (20 ~ 500) mg / mL were significantly lower than those of the corresponding concentrations of cetux Mab group (all P <0.01). Conclusion The IGF-ⅠR pathway may affect the proliferation of HepG2 cells induced by cetuximab, which may be one of the mechanisms of resistance to cetuximab in hepatocellular carcinoma cell lines.