肿瘤药学
腫瘤藥學
종류약학
ANTI-TUMOR PHARMACY
2013年
2期
92-95
,共4页
刘胜姿%谭宇婷%刘英姿%刘飞%周源*
劉勝姿%譚宇婷%劉英姿%劉飛%週源*
류성자%담우정%류영자%류비%주원*
乳腺癌%5,7-二甲氧基黄酮%凋亡%14-3-3σ
乳腺癌%5,7-二甲氧基黃酮%凋亡%14-3-3σ
유선암%5,7-이갑양기황동%조망%14-3-3σ
Breast cancer%5,7-DMF%Apoptosis%14-3-3σ
目的探讨5,7-二甲氧基黄酮(5,7-DMF)对人乳腺癌细胞凋亡的影响及其可能机制.方法体外培养乳腺癌 MDA-MB-453、MCF-7细胞和永生化人乳腺上皮 HBL-100细胞,经5,7-DMF 处理后,通过 MTT 法测定细胞活力;碘化丙啶(PI)染色流式细胞术(FCM)分析细胞凋亡率;甲基化特异性聚合酶链反应(MSP)检测14-3-3σ基因甲基化状态;Western blotting 分析14-3-3σ蛋白表达水平.结果5,7-DMF 对 MDA-MB-453细胞活性的抑制作用最强;不同浓度(5、10和20μmol·L-1)5,7-DMF 作用48小时后,可显著诱导 MDA-MB-453细胞凋亡,其细胞内14-3-3σ基因甲基化水平显著升高,而14-3-3σ蛋白表达水平显著降低.结论5,7-DMF 可诱导乳腺癌 MDA-MB-453细胞凋亡,其机制可能与促进14-3-3σ基因的甲基化和降低其蛋白表达有关.
目的探討5,7-二甲氧基黃酮(5,7-DMF)對人乳腺癌細胞凋亡的影響及其可能機製.方法體外培養乳腺癌 MDA-MB-453、MCF-7細胞和永生化人乳腺上皮 HBL-100細胞,經5,7-DMF 處理後,通過 MTT 法測定細胞活力;碘化丙啶(PI)染色流式細胞術(FCM)分析細胞凋亡率;甲基化特異性聚閤酶鏈反應(MSP)檢測14-3-3σ基因甲基化狀態;Western blotting 分析14-3-3σ蛋白錶達水平.結果5,7-DMF 對 MDA-MB-453細胞活性的抑製作用最彊;不同濃度(5、10和20μmol·L-1)5,7-DMF 作用48小時後,可顯著誘導 MDA-MB-453細胞凋亡,其細胞內14-3-3σ基因甲基化水平顯著升高,而14-3-3σ蛋白錶達水平顯著降低.結論5,7-DMF 可誘導乳腺癌 MDA-MB-453細胞凋亡,其機製可能與促進14-3-3σ基因的甲基化和降低其蛋白錶達有關.
목적탐토5,7-이갑양기황동(5,7-DMF)대인유선암세포조망적영향급기가능궤제.방법체외배양유선암 MDA-MB-453、MCF-7세포화영생화인유선상피 HBL-100세포,경5,7-DMF 처리후,통과 MTT 법측정세포활력;전화병정(PI)염색류식세포술(FCM)분석세포조망솔;갑기화특이성취합매련반응(MSP)검측14-3-3σ기인갑기화상태;Western blotting 분석14-3-3σ단백표체수평.결과5,7-DMF 대 MDA-MB-453세포활성적억제작용최강;불동농도(5、10화20μmol·L-1)5,7-DMF 작용48소시후,가현저유도 MDA-MB-453세포조망,기세포내14-3-3σ기인갑기화수평현저승고,이14-3-3σ단백표체수평현저강저.결론5,7-DMF 가유도유선암 MDA-MB-453세포조망,기궤제가능여촉진14-3-3σ기인적갑기화화강저기단백표체유관.
@@@@Objective To investigate the effects of 5, 7-DMF on the apoptosis of human breast cancer cells and its possible mechanisms. Methods Human breast cancer MDA-MB-453 cells, MCF-7 cells and human immortalized mammary epi-thelial HBL-100 cells were cultured in vitro. After treated with 5, 7-DMF, the cell viability was measured by MTT assay, and the rate of apoptosis was detected by using flow cytometry with PI staining. The methylation status of 14-3-3σ gene was determined by methlation specific PCR (MSP). The expression of 14-3-3σ protein was analyzed by Western blotting. Re-sults 5,7-DMF showed the strongest activity against MDA-MB-453 cells in vitro. After treated for 48 h, 5,7-DMF (5, 10 and 20 μmol·L-1) markedly induced the apoptosis of MDA-MB-453 cells, and the level of methylated 14-3-3σ gene was significantly increased, while the expression of 14-3-3σ protein was significantly decreased. Conclusion 5,7-DMF could induce the apoptosis of breast cancer MDA-MB-453 cells. Its mechanism may be related with the induction of the methyla-tion of 14-3-3σgene and the decrease of the expression of 14-3-3σprotein.