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目的:研究多肽K237对体外培养的雄激素非依赖性前列腺癌PC-3M细胞的抑制作用,及其可能的作用机制。方法:将培养的PC-3M细胞分为4组:实验组(分别以50、100、200μmol/L的多肽K237处理48h)和对照组(K237浓度为0μmol/L),采用MTT法观察多肽K237对前列腺癌PC-3M细胞增殖的影响,用RT-PCR法检测bax、bcl-2mRNA表达的变化。结果:不同浓度的多肽K237处理48h后,PC-3M细胞形状变圆,体积变小,胞质透亮度下降,部分细胞脱落悬浮于培养液中。在50、100、200μmol/L的多肽K237作用48h后,MTT法检测的细胞生长抑制率分别为(12.6±0.95)%、(17.8±0.99)%、(27.2±1.12)%。RT-PCR结果显示:50、100、200μmol/L实验组和对照组的bax/β-actin值分别为0.919±0.071、0.971±0.083、0.992±0.102,(0.889±0.06),bcl-2/β-actin值分别为0.896±0.085、0.791±0.084、0.764±0.702,0.922±0.097,3组中上述两项指标均较对照组有明显变化(P均<0.01),其中,baxmRNA表达水平上调,而bcl-2mRNA表达水平下调,上述作用呈现剂量效应关系。结论:多肽K237可能通过影响bax、bcl-2mRNA的表达来诱导PC-3M细胞凋亡,从而抑制前列腺癌细胞的增殖。
Objective: To study the inhibitory effect of K237 on androgen-independent prostate cancer PC-3M cells cultured in vitro and its possible mechanism. Methods: The cultured PC-3M cells were divided into four groups: experimental group (treated with 50,100 and 200μmol / L of polypeptide K237 for 48h) and control group (K237 concentration of 0μmol / L) On prostate cancer PC-3M cell proliferation, using RT-PCR assay bax, bcl-2mRNA expression changes. RESULTS: After treated with different concentrations of K237 peptide for 48 hours, the shape of PC-3M cells became round, the volume became smaller, the translocation of cytoplasm decreased, and some cells were suspended and suspended in culture medium. After treated with K237 at 50,100 and 200μmol / L for 48h, the cell growth inhibition rates were (12.6 ± 0.95)%, (17.8 ± 0.99)% and (27.2 ± 1.12)%, respectively. The results of RT-PCR showed that the values of bax / β-actin in the groups of 50, 100 and 200 μmol / L were 0.919 ± 0.071, 0.971 ± 0.083 and 0.992 ± 0.102, respectively (0.889 ± 0.06) and bcl-2 / β -actin values were 0.896 ± 0.085,0.791 ± 0.084,0.764 ± 0.702,0.922 ± 0.097, 3 groups of the above two indicators were significantly changed compared with the control group (P <0.01), of which, bax mRNA expression increased, and The expression of bcl-2mRNA was down-regulated, and the above effects showed a dose-response relationship. Conclusion: K237 polypeptide may induce the apoptosis of PC-3M cells by affecting the expression of bax and bcl-2 mRNA, thereby inhibiting the proliferation of prostate cancer cells.