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Transcription factor SOX2 contributes to nonalcoholic fatty liver disease development by regulating the expression of the fatty acid transporter CD36
FEBS Letters ( IF 3.0 ) Pub Date : 2021-09-18 , DOI: 10.1002/1873-3468.14193
Chen Shen 1 , Jin Hong Chen 1 , Ha Ram Oh 1 , Ji Hyun Park 1
Affiliation  

Nonalcoholic fatty liver disease (NAFLD) can lead to hepatocellular carcinoma (HCC). The level of the transcription factor SOX2 correlates with HCC progression, but its role in fat accumulation remains unclear. Here, a high-fat diet, with and without fructose, significantly upregulated SOX2 in murine liver tissue. Treatment with free fatty acids (FFAs) and fructose upregulated SOX2 in murine FL83B hepatocytes. SOX2 overexpression or knockdown regulated triglyceride synthesis and lipid accumulation after FFA stimulation. CD36, a fatty acid transporter, and Yes-associated protein (YAP), a downstream molecule of the Hippo signaling pathway, were upregulated by FFA/fructose in vivo and in vitro. Transcriptional regulation of CD36 by SOX2 suggested the involvement of CD36 in SOX2-mediated hepatic steatosis. Thus, SOX2 may be a target to prevent NAFLD development.

中文翻译:


转录因子 SOX2 通过调节脂肪酸转运蛋白 CD36 的表达促进非酒精性脂肪肝的发展



非酒精性脂肪肝(NAFLD)可导致肝细胞癌(HCC)。转录因子 SOX2 的水平与 HCC 进展相关,但其在脂肪堆积中的作用仍不清楚。在这里,含有或不含果糖的高脂肪饮食显着上调了小鼠肝组织中的 SOX2。游离脂肪酸 (FFA) 和果糖治疗上调小鼠 FL83B 肝细胞中的 SOX2。 SOX2 过表达或敲低可调节 FFA 刺激后的甘油三酯合成和脂质积累。 CD36(一种脂肪酸转运蛋白)和 Yes 相关蛋白(YAP)(Hippo 信号通路的下游分子)在体内体外均被 FFA/果糖上调。 SOX2 对 CD36 的转录调节表明 CD36 参与 SOX2 介导的肝脂肪变性。因此,SOX2可能是预防NAFLD发展的目标。
更新日期:2021-10-12
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