Takahashi N, Okumura T, Motomura W, Fujimoto Y, Kawabata I, Kohgo Y
Third Department of Internal Medicine, Asahikawa Medical College, Japan.
FEBS Lett. 1999 Jul 16;455(1-2):135-9. doi: 10.1016/s0014-5793(99)00871-6.
We investigated the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and the role of PPARgamma in cell growth in human gastric cancer cells. Reverse transcription-polymerase chain reaction, Northern blot and Western blot analyses showed that a human gastric cancer cell line, MKN45, expressed PPARgamma mRNA and protein. Luciferase assay in MKN45 cells showed that troglitazone, a selective ligand for PPARgamma, transactivated the transcription of a peroxisome proliferator response element-driven promoter. Troglitazone or pioglitazone, selective ligands for PPARgamma, inhibited the growth of MKN45 cells in a dose-dependent manner. Co-incubation of MKN45 cells with troglitazone induced DNA ladder formation. These results suggest that human gastric cancer cells express PPARgamma and that activation of PPARgamma inhibits cell growth and induces apoptosis in gastric cancer cells.
我们研究了过氧化物酶体增殖物激活受体γ（PPARγ）的表达及其在人胃癌细胞生长中的作用。逆转录-聚合酶链反应、Northern印迹和Western印迹分析表明，人胃癌细胞系MKN45表达PPARγ mRNA和蛋白。MKN45细胞中的荧光素酶测定表明，PPARγ的选择性配体曲格列酮可反式激活过氧化物酶体增殖物反应元件驱动的启动子的转录。曲格列酮或吡格列酮作为PPARγ的选择性配体，以剂量依赖的方式抑制MKN45细胞的生长。MKN45细胞与曲格列酮共同孵育可诱导DNA梯带形成。这些结果表明，人胃癌细胞表达PPARγ，PPARγ的激活可抑制胃癌细胞的生长并诱导其凋亡。
