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目的探讨干扰IGF-1R的表达对口腔鳞状细胞癌增殖、分化及凋亡的影响。方法 Western blot检测IGF-1R在口腔鳞状细胞癌中的表达;将NC-siRNA、IGF-1R-siRNA转染口腔鳞状细胞癌CAL27细胞,未转染任何siRNA作为对照组,细胞转染48 h后,Western blot检测IGF-1R、Id-1、c-myc、Cleaved caspase3、p-AKT、p-m TOR蛋白表达;CCK8实验检测细胞增殖;流式细胞仪检测细胞凋亡。结果 IGF-1R在口腔鳞状细胞癌中的表达显著高于癌旁组织(P<0.01);IGF-1R-siRNA组细胞中IGF-1R蛋白表达显著低于对照组(P<0.01);NC-siRNA组细胞存活率、细胞凋亡率及Id-1、c-myc、Cleaved caspase3、p-AKT、p-m TOR蛋白表达与对照组差异不显著(P>0.05),IGF-1R-siRNA组细胞存活率及Id-1、c-myc、p-AKT、p-m TOR蛋白表达显著低于对照组,细胞凋亡率及Cleaved caspase3蛋白表达显著高于对照组(P<0.01)。结论 IGF-1R在口腔鳞状细胞癌中高表达,抑制IGF-1R的表达能显著降低细胞增殖及分化,并促进细胞凋亡,其机制与AKT/m TOR信号通路调控有关。
Objective To investigate the effect of interfering with the expression of IGF-1R on the proliferation, differentiation and apoptosis of oral squamous cell carcinoma. Methods Western-blot was used to detect the expression of IGF-1R in oral squamous cell carcinoma. NC-siRNA and IGF-1R-siRNA were transfected into oral squamous cell carcinoma CAL27 cells without any siRNA as control group. h, Western blot was used to detect the protein expression of IGF-1R, Id-1, c-myc, Cleaved caspase3, p-AKT and pm TOR. Cell proliferation was detected by CCK8 assay and apoptosis was detected by flow cytometry. Results The expression of IGF-1R in oral squamous cell carcinoma was significantly higher than that in adjacent non-cancerous tissues (P <0.01). The expression of IGF-1R in IGF-1R-siRNA group was significantly lower than that in control group (P <0.01) The mRNA and protein expressions of Id-1, c-myc, Cleaved caspase3, p-AKT and pm TOR in the siRNA group were not significantly different from those in the control group (P> 0.05) The survival rate and the expressions of Id-1, c-myc, p-AKT and pm TOR were significantly lower than those of the control group. The apoptosis rate and the expression of Cleaved caspase 3 protein were significantly higher than those of the control group (P <0.01). Conclusion IGF-1R is overexpressed in oral squamous cell carcinoma, and the inhibition of IGF-1R expression can significantly reduce cell proliferation and differentiation and promote apoptosis. The mechanism is related to the regulation of AKT / m TOR signaling pathway.