首页> 中文期刊> 《肿瘤学与转化医学(英文)》 >Cis9,trans11和trans10,cis12-CLA诱导乳腺癌细胞MCF-7凋亡机制的研究(英文)

Cis9,trans11和trans10,cis12-CLA诱导乳腺癌细胞MCF-7凋亡机制的研究(英文)

         

摘要

Objective:The aim of the study was to explore the activities of cis9,trans11-CLA(C9,t11-CLA) and trans10,cis12-CLA(t10,c12-CLA) inhibiting tumor,and investigate their relationships with PPARγ and apoptotic proteins,and mechanism of anti-cancer.Methods:The inhibitory rate,cell growth curve and apoptotic morphological observation of MCF-7 cells were obtained by MTT assay,trypan blue staining and Hoechst33342 fluorescence staining.The apoptotic rate and cell cycle were detected with flow cytometry.Transcriptional level of genes was detected with RT-PCR semi-quantitative method,and Western blot was performed to detect proteins levels.Results:The two CLA isomers could reduce cell proliferation(P < 0.05),increase apoptotic rate(P < 0.05),and increase obviously the transcriptional and protein levels of PPARγ(P < 0.01).The synchronism and correlation between the effects of CLA to PPARγ and apoptotic proteins Bax,Bcl-2,Caspase 3 changes were found with the dose-and time-dependent manners.There was cooperative relation between the levels of PPARγ and the rates of Bax/Bcl-2,Caspase 3(small fragment) by experiments of PPARγ inhibitor GW9662 and ligand Rosiglitazone.Conclusion:The apoptotic pathway of PPARγ-Bcl-2-Caspase 3 signaling was found.The C9,t11-CLA and t10,c12-CLA could inhibit MCF-7 cell proliferation and promote apoptosis via activating PPARγ-Bcl-2-Caspase 3 pathway.CLA may be a kind of activator of PPARγ.

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