摘要
Peroxisome 激活 proliferator 的受体鲸鱼群妈(PPAR γ) coactivator-1 高山哈(PGC-1 α) coactivates 多重抄写因素并且调整几个代谢过程。Thecurrent 学习在人的上皮的卵巢的癌症房间在 apoptosis 的正式就职调查了 PGC-1 α的角色。在人的卵巢和人的卵巢的上皮的肿瘤之间的 PGC-1 α信使 rna 水平被量的 RT-PCR 检验。更少的 PGC-1 α表示与正常卵巢相比在恶意的肿瘤的表面上皮被发现。在人的上皮的卵巢的癌症房间线 Ho-8910 的 PGC-1 α的 Overexpression 通过 Bcl-2 和 Bax 表示的协调规定导致了房间 apoptosis。Microarray 分析证实 PGC-1 α戏剧性地在 Ho-8910 房间影响了 apoptosis 相关的基因。 Mitochondrial 功能的试金证明 apoptosis 的正式就职通过由细胞色素 c.Furthermore 的版本的终端阶段，导致的 apoptosis 部分是，然而并非完全，由 PPAR γa ntagonist ( GW9662 )堵住了的 PGC-1 α-，并且由 siRNA 的 PPAR γ 表示的抑制也在 Ho-8910 房间禁止了 PGC-1 α- inducedapoptosis 。这些数据建议 PGC-1 α通过 aPPAR γ - 依赖者小径施加了它的效果。我们的调查结果显示 PGC-1 α涉及 apoptotic signaltransduction 小径， PGC-1 α的 down 规定可以是在支持上皮的卵巢的癌症生长和前进的一个关键点。
Peroxisome proliferator-activated receptor gamma （PPAR）,） coactivator-1 alpha （PGC-1α） coactivates multiple transcription factors and regulates several metabolic processes. The current study investigated the role of PGC-1α in the induction of apoptosis in human epithelial ovarian cancer cells. The PGC-1α mRNA level between human ovaries and human ovarian epithelial tumors was examined by quantitative RT-PCR. Less PGC- 1α expression was found in the surface epithelium of malignant tumors compared with normal ovaries. Overexpression of PGC-1α in human epithelial ovarian cancer cell line Ho-8910 induced cell apoptosis through the coordinated regulation of Bcl-2 and Bax expression. Microarray analyses confirmed that PGC-1α dramatically affected the apoptosis-related genes in Ho-8910 cells. Mitochondrial functional assay showed that the induction of apoptosis was through the terminal stage by the release of cytochrome c. Furthermore, PG-C- 1 α-induced apoptosis was partially, but not completely, blocked by PPAR）, antagonist （GW9662）, and suppression of PPAR）, expression by siRNA also inhibited PGC-1α-induced apoptosis in Ho-8910 cells. These data suggested that PGC-1α exerted its effect through a PPARγ-dependent pathway. Our findings indicated that PGC-1α was involved in the apoptotic signal transduction pathways and downregulation of PGC-1α may be a key point in promoting epithelial ovarian cancer growth and progression.
基金
This work was supported by grants from the National Natural Science Foundation of China （No. 30225037, 30400538, 30471991,30570731）；the 973 Program of China （No. 2006CB503909, 2004CB518603）；the ＂111＂ Project, and the Natural Science Foundation of Jiangsu Province （No. BK2004082, BK2006714）.
