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目的:观察染料木黄酮(genistein)对前列腺癌细胞PC-3生物学行为的影响,探讨genistein预防前列腺癌的可能性。方法:用MTT法绘制生长曲线,观察0,10,20,40μmol/L的Genistein对PC-3细胞生长能力的影响;PC-3细胞经Genistein处理3d后,流式细胞术观察Genistein对前列腺癌细胞PC-3细胞周期的影响,Transwell小室法重建基底膜侵袭模型研究Genistein处理后细胞侵袭性的改变。结果:经Genistein处理后,PC-3细胞的生长受到抑制,作用3d时的药物半数致死量(IC50)为25μmol/L;细胞周期改变主要为G2/M阻滞,凋亡率(AI)明显增加,0,10,20,40μmol/L组的G2/M的百分比和AI分别为14.9%,27.4%,33.1%,31.9%和0,6.5%,14.2%,25.4%。侵袭能力分别下降到未加药组的31.8%,8.6%和3.96%。结论:Genistein通过引起PC-3细胞G2/M阻滞,诱导PC-3细胞凋亡,从而抑制PC-3细胞的恶性增殖以及降低PC-3细胞的侵袭能力可能是Genistein降低前列腺癌的发病率的一个重要原因。Genistein有可能成为预防前列腺癌的药物之一。
Objective: To observe the effect of genistein on the biological behavior of prostate cancer cell PC-3 and to explore the possibility of genistein in preventing prostate cancer. METHODS: The growth curve was plotted with MTT method and the effects of Genistein at 0, 10, 20, and 40 μmol/L on the growth of PC-3 cells were observed. After 3 days of PC-3 cells treated with Genistein, Genistein on prostate cancer was observed by flow cytometry. Effect of cell cycle of PC-3 cell, transwell chamber reconstruction of basement membrane invasion model to study the changes of cell invasiveness after Genistein treatment. RESULTS: After treated with Genistein, the growth of PC-3 cells was inhibited. The IC50 was 3 μmol/L at 3 days. The cell cycle changes were mainly G2/M arrest and the apoptosis rate (AI) was obvious. The percentages of G2/M and AI in the 0, 10, 20, and 40 μmol/L groups were 14.9%, 27.4%, 33.1%, 31.9%, and 0, 6.5%, 14.2%, and 25.4%, respectively. The invasive ability dropped to 31.8%, 8.6%, and 3.96%, respectively, in the unmedicated group. CONCLUSION: Genistein induces apoptosis of PC-3 cells by inducing G2/M arrest of PC-3 cells, thereby inhibiting the malignant proliferation of PC-3 cells and reducing the invasion ability of PC-3 cells. It may be that Genistein reduces the incidence of prostate cancer. An important reason. Genistein may become one of the drugs to prevent prostate cancer.