Chondrosarcoma and peroxisome proliferator-activated receptor.
Chondrosarcoma and peroxisome proliferator-activated receptor.
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软骨肉瘤和过氧化物酶体增殖物激活受体。
DOI：
10.1155/2008/250568
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发表时间：
2008
期刊：
影响因子：
2.9
通讯作者：
Ozaki T
中科院分区：
文献类型：
--
作者：
Nishida K;Kunisada T;Shen ZN;Kadota Y;Hashizume K;Ozaki T
PPARγ配体诱导癌细胞分化和凋亡是治疗恶性肿瘤的新途径。软骨肉瘤（恶性软骨肿瘤）和OUMS-27细胞（从III级人软骨肉瘤建立的细胞系）表达PPARγ。PPARγ配体以剂量依赖性方式抑制细胞增殖，诱导OUMS-27细胞凋亡。高级别软骨肉瘤在体内表达更多的抗凋亡Bcl-xL。15d-PGJ2 （PPARγ最有效的内源性配体）处理OUMS-27后，下调Bcl-xL的表达，诱导促凋亡Bax的短暂上调，从而加速细胞色素c从线粒体向胞质溶胶的释放，诱导caspase依赖性凋亡。15d-PGJ2诱导人软骨肉瘤细胞中CDK抑制剂p21蛋白的表达，可能参与了抑制细胞增殖的机制。这些发现提示PPARγ配体靶向治疗可能是一种治疗软骨肉瘤的新策略。
Induction of differentiation and apoptosis in cancer cells by ligands of PPARγ is a novel therapeutic approach to malignant tumors. Chondrosarcoma (malignant cartilage tumor) and OUMS-27 cells (cell line established from grade III human chondrosarcoma) express PPARγ. PPARγ ligands inhibited cell proliferation in a dose-dependent manner, and induced apoptosis of OUMS-27. The higher-grade chondrosarcoma expressed a higher amount of antiapoptotic Bcl-xL in vivo. The treatment of OUMS-27 by 15d-PGJ2, the most potent endogenous ligand for PPARγ, downregulated expression of Bcl-xL and induced transient upregulation of proapoptotic Bax, which could accelerate cytochrome c release from mitochondria to the cytosol, followed by induction of caspase-dependent apoptosis. 15d-PGJ2 induced the expression of CDK inhibitor p21 protein in human chondrosarcoma cells, which appears to be involved in the mechanism of inhibition of cell proliferation. These findings suggest that targeted therapy with PPARγ ligands could be a novel strategy against chondrosarcoma.
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影响因子：
2.8
作者：
Chansky, H;Robbins, JR;Sandell, LJ
通讯作者：
Sandell, LJ
影响因子：
4.8
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影响因子：
3.3
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DORFMAN, HD
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作者：
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通讯作者：
Ninomiya, Y
影响因子：
5
作者：
Gil-Benso, R;Lopez-Gines, C;Llombart-Bosch, A
通讯作者：
Llombart-Bosch, A