Elnemr A, Ohta T, Iwata K, Ninomia I, Fushida S, Nishimura G, Kitagawa H, Kayahara M, Yamamoto M, Terada T, Miwa K
Department of Surgery II, School of Medicine, Kanazawa University, Kanazawa 920-0934, Japan.
Int J Oncol. 2000 Dec;17(6):1157-64. doi: 10.3892/ijo.17.6.1157.
The aim of this study was to examine whether a specific PPARgamma ligand can inhibit the growth of human pancreatic cancer cells through induction of terminal differentiation. PPARgamma was expressed in five human pancreatic cancer cell lines: Capan-1, AsPC-1, BxPC-3, PANC-1, and MIA PaCa-2. Treatment of these cells with a specific PPARgamma ligand, thiazolidinedione (TZD), resulted in inhibition of both cellular and clonogenic growth, and G1 cell cycle arrest. Finally, thiazolidinedione treatment resulted in induction of p21WAF-1 and increased expression of differentiation markers. These results suggest that thiazolidinedione treatment inhibits growth and induces cellular differentiation in pancreatic cancer cells and thereby reduces their development in favor of differentiated and stable cell phenotype.
本研究的目的是检测一种特定的过氧化物酶体增殖物激活受体γ（PPARγ）配体是否能通过诱导终末分化来抑制人胰腺癌细胞的生长。PPARγ在五种人胰腺癌细胞系中表达：Capan-1、AsPC-1、BxPC-3、PANC-1和MIA PaCa-2。用一种特定的PPARγ配体噻唑烷二酮（TZD）处理这些细胞，导致细胞生长和克隆形成生长均受到抑制，并使细胞周期停滞于G1期。最后，噻唑烷二酮处理导致p21WAF-1的诱导和分化标志物表达增加。这些结果表明，噻唑烷二酮处理可抑制胰腺癌细胞的生长并诱导细胞分化，从而有利于分化和稳定的细胞表型，减少其发展。
