过氧化物酶体增殖物激活受体可能有助于肝癌的发病机制。
PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma.
机构信息
Division of Gastroenterology, Tohoku University Hospital, 1-1 Seiryo-Machi, Aoba-ku, Sendai City, Miyagi 980-8574, Japan.
出版信息
PPAR Res. 2012;2012:574180. doi: 10.1155/2012/574180. Epub 2012 Dec 16.
Abstract
Viral hepatitis with hepatitis C virus or hepatitis B virus and chronic liver disease such as alcoholic or nonalcoholic steatohepatitis are critical factors in the development of hepatocellular carcinoma (HCC). Furthermore, diabetes is known as an independent risk factor for HCC. Peroxisome proliferator-activated receptor (PPAR) is known to have an important role in fatty liver, and the mechanism of carcinogenesis has been clarified. PPAR controls ligand-dependent transcription, and three subtypes (α, δ, and γ) in humans are known. PPARs could contribute to the mechanisms of cell cycling, anti-inflammatory responses, and apoptosis. Therefore, to clarify the pathogenesis of HCC, we should examine PPAR signaling. In this paper, we have summarized the relevance of PPARs to the pathogenesis of HCC and cancer stem cells and possible therapeutic options through modifying PPAR signaling.
摘要
病毒性肝炎，包括丙型肝炎病毒或乙型肝炎病毒，以及慢性肝病，如酒精性或非酒精性脂肪性肝炎，是肝细胞癌（HCC）发展的关键因素。此外，糖尿病被认为是 HCC 的一个独立危险因素。过氧化物酶体增殖物激活受体（PPAR）已知在脂肪肝中具有重要作用，其致癌机制已得到阐明。PPAR 控制配体依赖性转录，在人类中已知有三种亚型（α、δ 和 γ）。PPAR 可能有助于细胞周期、抗炎反应和细胞凋亡的机制。因此，为了阐明 HCC 的发病机制，我们应该检查 PPAR 信号。在本文中，我们总结了 PPAR 与 HCC 发病机制和癌症干细胞的相关性，以及通过修饰 PPAR 信号的可能治疗选择。
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