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目的探讨氯化两面针碱对前列腺癌细胞PC-3增殖及凋亡的影响作用。方法采用MTT、细胞划痕和Transw ell侵袭实验评估氯化两面针碱对人前列腺癌细胞PC-3增殖与侵袭的影响;流式细胞术检测氯化两面针碱对PC-3细胞凋亡的影响;免疫印迹检测AKT/m TOR及细胞凋亡蛋白B细胞淋巴瘤基因-2相关X蛋白(Bax)和B细胞淋巴瘤基因-2(Bcl-2)的表达,应用PI3K通路抑制剂LY294002探讨抑制AKT通路对前列腺癌细胞PC-3的影响。结果氯化两面针碱能抑制PC-3细胞的增殖与侵袭,且具有剂量依赖性(P<0.01)。氯化两面针碱可下调Bcl-2、而上调Bax的蛋白表达,Bax/Bcl-2比例明显上升(P<0.01),抑制AKT和m TOR通路的磷酸化,诱导前列腺癌细胞PC-3凋亡。联合应用LY294002发现,抑制AKT通路可增强氯化两面针碱对前列腺癌细胞PC-3增殖和侵袭的抑制作用。结论氯化两面针碱能够抑制前列腺癌细胞PC-3的增殖与侵袭,诱导其凋亡,并通过抑制AKT/m TOR磷酸化发挥其抗前列腺癌作用,可作为一种潜在治疗前列腺癌的药物。
Objective To investigate the effects of nitidine chloride on the proliferation and apoptosis of prostate cancer cell line PC-3. Methods The effects of nitidine chloride on the proliferation and invasion of human prostate cancer cell line PC-3 were evaluated by MTT assay, cell scratch assay and Transwell assay. Flow cytometry was used to detect the apoptosis of PC-3 cells induced by nitidine chloride The expression of AKT / m TOR and Bcl-2 and Bcl-2 were detected by Western blot, and the PI3K pathway inhibitor LY294002 was used to investigate the expression of AKT / m TOR and apoptosis protein B cell lymphoma Inhibition of AKT pathway on prostate cancer cells PC-3. Results Nitidine chloride could inhibit the proliferation and invasion of PC-3 cells in a dose-dependent manner (P <0.01). Bcl-2 was down-regulated by nitidine chloride chloride, while the protein expression of Bax was up-regulated. The proportion of Bax / Bcl-2 was significantly increased (P <0.01), and the phosphorylation of AKT and mTOR pathway was inhibited. Death. Combined use of LY294002 found that inhibition of AKT pathway can enhance the nitidine chloride on Prostate cancer cell PC-3 proliferation and invasion inhibition. CONCLUSION: Nitidine chloride can inhibit the proliferation and invasion of PC-3 cells and induce apoptosis of PC-3 cells. It can also be used as a potential drug for the treatment of prostate cancer by inhibiting AKT / mTOR phosphorylation .