肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2012年
4期
235-238
,共4页
顾金花%陈玲%陆培华%陈敏斌
顧金花%陳玲%陸培華%陳敏斌
고금화%진령%륙배화%진민빈
乳腺肿瘤%腺苷酸激酶%多柔比星%细胞增殖
乳腺腫瘤%腺苷痠激酶%多柔比星%細胞增殖
유선종류%선감산격매%다유비성%세포증식
Breast neoplasms%Adenylate kinase%Doxorubicin%Cell proliferation
目的 研究多柔比星对乳腺癌MCF-7细胞增殖的影响,并探讨腺苷酸活化蛋白激酶(AMPK)在其中的作用.方法 分别用AMPK激活剂AICAR、siRNA敲低AMPK表达(AMPK siRNA)、AMPK抑制剂复合物C(AMPKi)联合多柔比星(DOX)对MCF-7细胞进行处理,在不同时间通过Western blot方法检测AMPK、乙酰辅酶A羧化酶(ACC)、p38的活化,MTT检测细胞存活率间接反应细胞增殖.结果 DOX可诱导MCF-7细胞AMPK的活化,AICAR单独或联合DOX可诱导AMPK的激活及增加MCF-7细胞增殖抑制率,AICAR+ DOX组与DOX组细胞存活率分别为(17.7±1.6)％和(71.4±1.8)％(P＜0.001)；AMPKi或AMPK siRNA联合DOX后,p-AMPK及p-ACC表达明显下降,p38活化水平不受影响,MCF-7细胞增殖抑制率下降,AMPKi+DOX组与DOX组细胞存活率分别为(72.7±1.8)％和( 96.3±1.7)％(P＜0.001),AMPK siRNA +DOX组与错义siRNA+DOX组细胞存活率分别为(76.9±2.2)％和( 95.9±1.8)％(P＜0.001).结论 AMPK介导DOX诱导的抗乳腺癌细胞增殖.
目的 研究多柔比星對乳腺癌MCF-7細胞增殖的影響,併探討腺苷痠活化蛋白激酶(AMPK)在其中的作用.方法 分彆用AMPK激活劑AICAR、siRNA敲低AMPK錶達(AMPK siRNA)、AMPK抑製劑複閤物C(AMPKi)聯閤多柔比星(DOX)對MCF-7細胞進行處理,在不同時間通過Western blot方法檢測AMPK、乙酰輔酶A羧化酶(ACC)、p38的活化,MTT檢測細胞存活率間接反應細胞增殖.結果 DOX可誘導MCF-7細胞AMPK的活化,AICAR單獨或聯閤DOX可誘導AMPK的激活及增加MCF-7細胞增殖抑製率,AICAR+ DOX組與DOX組細胞存活率分彆為(17.7±1.6)％和(71.4±1.8)％(P＜0.001)；AMPKi或AMPK siRNA聯閤DOX後,p-AMPK及p-ACC錶達明顯下降,p38活化水平不受影響,MCF-7細胞增殖抑製率下降,AMPKi+DOX組與DOX組細胞存活率分彆為(72.7±1.8)％和( 96.3±1.7)％(P＜0.001),AMPK siRNA +DOX組與錯義siRNA+DOX組細胞存活率分彆為(76.9±2.2)％和( 95.9±1.8)％(P＜0.001).結論 AMPK介導DOX誘導的抗乳腺癌細胞增殖.
목적 연구다유비성대유선암MCF-7세포증식적영향,병탐토선감산활화단백격매(AMPK)재기중적작용.방법 분별용AMPK격활제AICAR、siRNA고저AMPK표체(AMPK siRNA)、AMPK억제제복합물C(AMPKi)연합다유비성(DOX)대MCF-7세포진행처리,재불동시간통과Western blot방법검측AMPK、을선보매A최화매(ACC)、p38적활화,MTT검측세포존활솔간접반응세포증식.결과 DOX가유도MCF-7세포AMPK적활화,AICAR단독혹연합DOX가유도AMPK적격활급증가MCF-7세포증식억제솔,AICAR+ DOX조여DOX조세포존활솔분별위(17.7±1.6)％화(71.4±1.8)％(P＜0.001)；AMPKi혹AMPK siRNA연합DOX후,p-AMPK급p-ACC표체명현하강,p38활화수평불수영향,MCF-7세포증식억제솔하강,AMPKi+DOX조여DOX조세포존활솔분별위(72.7±1.8)％화( 96.3±1.7)％(P＜0.001),AMPK siRNA +DOX조여착의siRNA+DOX조세포존활솔분별위(76.9±2.2)％화( 95.9±1.8)％(P＜0.001).결론 AMPK개도DOX유도적항유선암세포증식.
Objective To investigate the mechanism of anti-breast cancer cell proliferation induced by doxorubicin (DOX).Methods AMP-Activated Protein Kinase (AMPK) activator AICAR,AMPK siRNA,AMPK inhibitor compound C(AMPKi) and doxorubicin treated MCF-7 cells at different time points; AMPK,acetyl CoA carboxylase (ACC),p38 activation were detected by Western blot.MTT was used as cell viability assay. Results Doxorubicin-induced activation of AMPK, AMPK agonist (AICAR)or in combination with doxorubicin activated AMPK and increased MCF-7 cell proliferation rate [the difference of cell viability between group AICAR+DOX(17.7±1.6 ) ％ and group DOX(71.4±1.8 ) ％ was significant(P＜0.001)].After AMPKi or AMPK siRNA and doxorubicin combined administration, P-AMPK and P-ACC expression was significantly decreased,the level of p38 was not affected,and MCF-7 cell proliferation inhibition rate decreased [the cell viability of group AMPKi+DOX(72.7±1.8 ) ％ vs group DOX(96.3±1.7 ) ％,P＜0.001 ;group AMPK siRNA +DOX( 76.9±2.2 ) ％ vs group scramble siRNA+DOX(95.9±1.8) ％,P＜0.001].Conclusion AMPK is involved in doxorubicin-induced anti-breast cancer cell proliferation.
