MiR-205 modulates abnormal lipid metabolism of hepatoma cells via targeting acyl-CoA synthetase long-chain family member 1 (ACSL1) mRNA

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• 作者：Ming Cui ; Yue Wang ; Baodi Sun ; Zelin Xiao ; Lihong Ye ; Xiaodong Zhang
• 关键词：HCC ; hepatocellular carcinoma ; miRNA ; microRNA ; ACSL1 ; acyl-CoA synthetase long-chain family member 1 ; 3&prime ; UTR ; 3&prime ; untranslated region ; qRT-PCR ; quantitative real-time polymerase chain reaction ; RT-PCR ; reverse transcription-polymerase chain reaction ; HBx ; hepatitis B virus X protein
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：7 February, 2014
• 年：2014
• 卷：444
• 期：2
• 页码：270-275
• 全文大小：948 K

文摘

The abnormal lipid metabolism is considered as a hallmarker of tumorigenesis. Liver is the central organ for metabolic homeostasis. Hence, the development of hepatocellular carcinoma (HCC) always exhibits alterations of metabolism. MicroRNAs emerge as key post-transcriptional modulators of gene expression in physiologic and pathologic states. Here, we aim to explore the mechanism of abnormal lipid metabolism of hepatoma cells. Previously, our group reported that miR-205 as a tumor suppressor was down-regulated in HCC. Therefore, we supposed that miR-205 might be involved in the event. Interestingly, in this study we uncover that miR-205 deregulates lipid metabolism in HCC through targeting acyl-CoA synthetase long-chain family member 1 (ACSL1) mRNA, which is an important and abundant lipid metabolism enzyme in liver. We identified that miR-205 was able to down-regulate ACSL1 via targeting its 3鈥睻TR in the cells. Oil red O staining showed that miR-205 disordered the lipogenesis in hepatoma cells and anti-miR-205 resulted in the accumulation of triglyceride in the cells depending on ACSL1. Moreover, we validated that the low levels of miR-205 were negatively related to high levels of ACSL1 in clinical HCC tissues. The expression levels of ACSL1 and its metabolite triglyceride levels were remarkably increased in hepatitis B virus X protein (HBx)-induced liver cancer tissues from the HBx transgenic mice model. Thus, we conclude that miR-205-targeted ACSL1 may contribute to the abnormal lipid metabolism of liver cancer. Our finding provides new insights into the dysregulation of lipid metabolism in HCC mediated by miR-205 targeting ACSL1 mRNA.