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目的探讨ERK1/2、PI3K-Akt途径在雌激素17β-雌二醇(17β-estradiol,E2)促进人甲状腺未分化癌FRO细胞增殖中的作用及其机制。方法分别用E2、雌激素受体抑制剂ICI182780(ICI)、ERK1/2抑制剂PD98059(PD)和PI3K-Akt抑制剂LY294002(LY)单独或联合处理FRO细胞,MTT法检测细胞增殖率,Western blot法检测细胞ERα、ERβ、Bcl-2及Bax蛋白的表达水平。结果 E2可促进FRO细胞增殖及ERα、Bcl-2蛋白的表达,抑制Bax蛋白的表达;ICI可抑制Bcl-2蛋白的表达,对Bax蛋白的表达无明显影响;PD和LY可抑制E2对FRO细胞的上述作用。结论 E2可通过激活ERK1/2、PI3K-Akt通路,增加Bcl-2/Bax的比值,促进FRO细胞增殖。
Objective To investigate the role and mechanism of ERK1 / 2 and PI3K-Akt pathway in the proliferation of human thyroid carcinoma cell line FRO with 17β-estradiol (E2). Methods FRO cells were treated with E2, estrogen receptor inhibitor ICI182780 (ICI), ERK1 / 2 inhibitor PD98059 (PD) and PI3K-Akt inhibitor LY294002 (LY) separately or in combination. MTT assay was used to detect cell proliferation rate blot was used to detect the expression of ERα, ERβ, Bcl-2 and Bax. Results E2 could promote the proliferation of FRO cells and the expression of ERα and Bcl-2 protein, and inhibit the expression of Bax protein. ICI inhibited the expression of Bcl-2 protein and had no effect on the expression of Bax protein. PD and LY inhibited the effect of E2 on FRO The above effects of cells. Conclusion E2 can promote the proliferation of FRO cells by activating ERK1 / 2, PI3K-Akt pathway and increasing the ratio of Bcl-2 / Bax.