论文部分内容阅读
目的:探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂曲格列酮(TRG)对体外培养雌激素受体(ER)阴性乳腺癌MDA-MB-231细胞及ER+乳腺癌MCF-7细胞增殖的影响。方法:以不同浓度的TRG(0～50μmol/mL)分别处理体外培养的MDA-MB-231细胞和MCF-7细胞48h,MTT法检测细胞存活率;流式细胞术(FCM)检测细胞周期分布;蛋白质印迹法检测PPARγ和ER-α的表达。结果:MTT结果示TRG浓度≥5μmol/mL时MDA-MB-231细胞(P值分别为0.006、0.006、0.000和0.000)和MCF-7细胞(P值分别为0.007、0.006、0.004和0.001)的存活率降低。FCM检测结果表明,经TRG作用后肿瘤细胞主要集中在G1期。以上2种检测结果显示,MDA-MB-231细胞对TRG的敏感程度较MCF-7细胞高;蛋白质印迹法检测结果表明,TRG处理后的MDA-MB-231细胞中PPARγ蛋白的表达水平随药物浓度增加逐渐升高(相对强度分别为2.045、2.600和3.038),MCF-7细胞的ER-α表达水平则随药物浓度增加逐渐降低(相对强度分别为1.164、1.130和0.680)。结论:TRG对ER+和ER-乳腺癌细胞均有抑制作用,且ER-乳腺癌细胞对TRG更敏感。
Objective: To investigate the effect of peroxisome proliferator-activated receptor γ (PPARγ) agonist troglitazone (TRG) on the proliferation of estrogen receptor (ER) negative breast cancer MDA-MB-231 cells and ER + -7 cell proliferation. Methods: MDA-MB-231 cells and MCF-7 cells were treated with different concentrations of TRG (0-50 μmol / mL) for 48 h respectively. Cell viability was measured by MTT assay. Cell cycle distribution was analyzed by flow cytometry (FCM) ; Western blotting was used to detect the expression of PPARγ and ER-α. Results: MTT results showed that the percentage of MDA-MB-231 cells (P = 0.006, 0.006, 0.000 and 0.000, respectively) and MCF-7 cells (P values were 0.007, 0.006, 0.004 and 0.001, respectively) Survival rate decreased. FCM results showed that the tumor cells mainly concentrated in G1 phase after TRG treatment. The above two results showed that the sensitivity of MDA-MB-231 cells to TRG was higher than that of MCF-7 cells. Western blotting showed that the expression of PPARγ protein in TRG-treated MDA-MB-231 cells was up- (Relative intensities were 2.045, 2.600 and 3.038, respectively). The expression of ER-α in MCF-7 cells gradually decreased with the increase of drug concentration (relative intensity was 1.164,1.130 and 0.680 respectively). Conclusion: TRG can inhibit both ER + and ER-breast cancer cells, and ER-breast cancer cells are more sensitive to TRG.