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目的观察胰岛素对前列腺癌LNCaP细胞系增殖、活力、迁移与侵袭能力的影响,并探讨其机制。方法胰岛素刺激LNCaP细胞后,采用实时荧光定量聚合酶链反应(Real-time PCR)、蛋白免疫印迹(Western blotting)、免疫细胞化学(ICC)法检测胰岛素受体表达变化;细胞计数法、四唑盐法(MTT)、细胞划痕、细胞侵袭实验(Transwell)检测细胞增殖、活力、迁移和侵袭能力;Western blotting检测Ras、ERK1/2、MEK1/2蛋白水平表达变化。结果胰岛素可促进LNCaP细胞胰岛素受体的表达,抑制其增殖、活力、迁移及侵袭能力,同时抑制其Ras的表达及ERK1/2、MEK1/2的磷酸化(P<0.05)。结论胰岛素可通过胰岛素受体抑制Ras-MEK-ERK信号通路的活化,从而抑制LNCaP细胞的增殖、活力、迁移及侵袭。
Objective To observe the effect of insulin on the proliferation, vitality, migration and invasion of prostate cancer cell line LNCaP and to explore its mechanism. Methods After LNCaP cells were stimulated with insulin, the expression of insulin receptor was detected by Real-time PCR, Western blotting and immunocytochemistry (ICC). Cell counting, The cell proliferation, viability, migration and invasion were evaluated by MTT assay, cell scratch assay and cell invasion assay (Transwell). The protein expression of Ras, ERK1 / 2 and MEK1 / 2 was detected by Western blotting. Results Insulin promoted the expression of insulin receptor and inhibited the proliferation, vitality, migration and invasion of LNCaP cells, and inhibited the expression of Ras and the phosphorylation of ERK1 / 2 and MEK1 / 2 (P <0.05). Conclusion Insulin can inhibit the proliferation, viability, migration and invasion of LNCaP cells by inhibiting the activation of Ras-MEK-ERK signaling pathway through insulin receptor.