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PPAR属于核受体超家族,与特异配体结合后调控一些基因的表达,这些受调控的基因涉及脂质的代谢,糖尿病以及肿瘤等多个方面.目的是研究PPARγ激动剂罗格列酮诱导结肠癌细胞HT-29凋亡及细胞周期阻滞的作用,并对其机制做相应的探讨.试验结果显示,罗格列酮可诱导HT-29细胞发生凋亡,并阻滞细胞于G1期,此效果伴随着Bcl-2的表达降低,p21的表达升高.罗格列酮在升高PPARγ表达的同时,也激活了细胞内ERK的传导通路.因此,罗格列酮是通过诱导结肠癌细胞凋亡及周期阻滞而发挥其抗肿瘤作用,此作用为PPARγ依赖的,并且与激活ERK通路有关.这些研究结果提示PPARγ有望成为结肠癌治疗的分子靶点.
PPAR belongs to the nuclear receptor superfamily and regulates the expression of some genes after binding with specific ligands, and these regulated genes are involved in lipid metabolism, diabetes and cancer, etc. The purpose is to study the PPARγ agonist rosiglitazone-induced Colon cancer cells HT-29 apoptosis and cell cycle arrest, and to explore its mechanism.Results showed that rosiglitazone could induce apoptosis of HT-29 cells and arrest cells in G1 phase , And this effect is associated with a decrease in the expression of Bcl-2 and an increase in p21.Rogasterone also activates the intracellular ERK pathway while increasing PPARy expression.Therefore, rosiglitazone induces colonic Cancer cell apoptosis and cycle arrest and exert its anti-tumor effect, the role of PPARγ-dependent, and activation of ERK pathway.These results suggest that PPARγ is expected to become a molecular target for the treatment of colon cancer.