CAJ | 학술논문

目的：探讨促性腺激素释放激素（ gonadotropin-releasing hormone ， GnRH）类似物曲普瑞林（ trip-torelin）对人乳腺癌细胞株MCF-7、MDA-MB-231细胞生长及细胞外信号调节蛋白激酶（ extracellular signal-regulated kinase， ERK）／丝裂原活化蛋白激酶（ mitogen-activated protein kinases ， MAPK）和磷脂酰肌醇-3-激酶（ phosphatidyli-nositol-3-kinase， PI3K）／蛋白激酶B（protein kinase B， Akt）信号通路中重要信号分子ERK1／2和Akt活化的影响。方法：使用不同浓度、不同时间的曲普瑞林刺激人乳腺癌MCF-7及MDA-MB-231细胞株，MTT法检测细胞增殖，流式细胞术检测细胞周期的分布，Western blotting检测Akt和ERK1／2的磷酸化程度。结果：曲普瑞林（10-5 mol／L）作用人乳腺癌MCF-7细胞192 h、曲普瑞林（10－4 mol／L）作用人乳腺癌MCF-7细胞168 h、192 h或曲普瑞林（10－4 mol／L）作用人乳腺癌MDA-MB-231细胞192 h可明显抑制细胞生长（ P＜0.05）；曲普瑞林（10－4 mol／L）作用人乳腺癌MCF-7和MDA-MB-231细胞192 h，ERK1／2的磷酸化程度均较正常对照组低，Akt的磷酸化程度较正常对照组高，但差异无统计学意义（ P＞0.05）。结论：GnRH类似物曲普瑞林对人乳腺癌细胞的抑制作用，不仅仅是通过对垂体激素的降调节机制，还可能产生直接抑制作用。但该抑制作用未涉及ERK／MAPK和PI3K／Akt信号通路。
목적：탐토촉성선격소석방격소（ gonadotropin-releasing hormone ， GnRH）유사물곡보서림（ trip-torelin）대인유선암세포주MCF-7、MDA-MB-231세포생장급세포외신호조절단백격매（ extracellular signal-regulated kinase， ERK）／사렬원활화단백격매（ mitogen-activated protein kinases ， MAPK）화린지선기순-3-격매（ phosphatidyli-nositol-3-kinase， PI3K）／단백격매B（protein kinase B， Akt）신호통로중중요신호분자ERK1／2화Akt활화적영향。방법：사용불동농도、불동시간적곡보서림자격인유선암MCF-7급MDA-MB-231세포주，MTT법검측세포증식，류식세포술검측세포주기적분포，Western blotting검측Akt화ERK1／2적린산화정도。결과：곡보서림（10-5 mol／L）작용인유선암MCF-7세포192 h、곡보서림（10－4 mol／L）작용인유선암MCF-7세포168 h、192 h혹곡보서림（10－4 mol／L）작용인유선암MDA-MB-231세포192 h가명현억제세포생장（ P＜0.05）；곡보서림（10－4 mol／L）작용인유선암MCF-7화MDA-MB-231세포192 h，ERK1／2적린산화정도균교정상대조조저，Akt적린산화정도교정상대조조고，단차이무통계학의의（ P＞0.05）。결론：GnRH유사물곡보서림대인유선암세포적억제작용，불부부시통과대수체격소적강조절궤제，환가능산생직접억제작용。단해억제작용미섭급ERK／MAPK화PI3K／Akt신호통로。
AIM:To investigate the effects of gonadotropin-releasing hormone ( GnRH) analogue on the growth of breast cancer cell lines MCF-7 and MDA-MB-231 in vitro and to explore the related mechanisms with PI 3K/Akt or ERK/MAPK pathways .METHODS: The proliferation of human breast cancer cell lines MCF-7 and MDA-MB-231 treatment with triptorelin was detected by MTT assay and the distribution of the cell cycle was determined by flow cytometry .The phosphorylation of the ERK 1/2 and Akt was evaluated by Western blotting .RESULTS:Triptorelin inhibited the prolifera-tion of MCF-7 cells at concentration of 10-5 mol/L after treated for 192 h or at concentration of 10 -4 mol/L after treated for 168 h and 192 h.Triptorelin inhibited the proliferation of MDA-MB-231 cells at concentration of 10 -4 mol/L after treated for 192 h (P<0.05).Treatment with triptorelin for 192 h at concentration of 10 -4 mol/L had no statistical significance effect on phosphorylation of ERK1/2 and Akt(P>0.05).CONCLUSION:Inhibitory effect of GnRH analogue triptorelin on human breast cancer cells is not just the connection with the down-regulation of pituitary hormone , but also a direct in-hibitory effect.The role may not be involved in the activation of ERK /MAPK and PI3K/Akt signaling pathways .