Antitumor action of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone in hepatocellular carcinoma.
Antitumor action of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone in hepatocellular carcinoma.
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DOI：
10.3892/ol.2015.3554
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发表时间：
2015-10
期刊：
影响因子：
2.9
通讯作者：
Li GX
中科院分区：
文献类型：
--
作者：
Bo QF;Sun XM;Liu J;Sui XM;Li GX
癌细胞凋亡抑制是肝癌的主要病理特征。罗格列酮（RGZ）是过氧化物酶体增殖物激活受体γ（PPAR-γ）的配体，可诱导肝癌细胞凋亡。然而，这种影响的机制仍有待阐明。本研究采用MTT法、流式细胞术和Western blotting法研究RGZ对HepG 2细胞活力和凋亡的影响，并探讨其作用机制。结果表明RGZ可降低HepG 2细胞的存活率并诱导细胞凋亡。RGZ诱导细胞凋亡的机制涉及激活的PPAR-γ（p-PPAR-γ）水平的增加和p85和Akt表达的降低。此外，PPAR-γ拮抗剂GW 9662可抑制RGZ对HepG 2细胞的作用。以上结果提示，RGZ通过激活PPAR-γ，抑制PI 3 K/Akt信号通路的激活，诱导HepG 2细胞凋亡。这些机制可能有助于使用RGZ在HepG 2细胞中的治疗的有利效果。
The inhibition of apoptosis in cancer cells is the major pathological feature of hepatic carcinoma. Rosiglitazone (RGZ), a ligand for peroxisome proliferator-activated receptor γ (PPAR-γ), has been shown to induce apoptosis in hepatic carcinoma cells. However, the mechanism underlying this effect remains to be elucidated. The present study aimed to investigate the effect of RGZ on cell viability and apoptosis, and its mechanisms in cultured HepG2 cells using MTT assay, flow cytometry and western blotting. The results revealed that treatment with RGZ may attenuate HepG2 cell viability and induce the apoptosis of the cells. The mechanism of RGZ-induced apoptosis involves an increase in the level of activated PPAR-γ (p-PPAR-γ) and a decrease in p85 and Akt expression. In addition, the PPAR-γ antagonist GW9662 suppressed the effect of RGZ in the HepG2 cells. Taken together, the results suggest that RGZ induces the apoptosis of HepG2 cells through the activation of PPAR-γ, suppressing the activation of the PI3K/Akt signaling pathway. Such mechanisms may contribute to the favorable effects of treatment using RGZ in HepG2 cells.