Upregulation of Superenhancer-Driven LncRNA FASRL by USF1 Promotes De Novo Fatty Acid Biosynthesis to Exacerbate Hepatocellular Carcinoma.
Upregulation of Superenhancer-Driven LncRNA FASRL by USF1 Promotes De Novo Fatty Acid Biosynthesis to Exacerbate Hepatocellular Carcinoma.
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USF1上调超增强子驱动的LncRNA FASRL促进从头脂肪酸生物合成，加剧肝细胞癌
DOI：
10.1002/advs.202204711
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发表时间：
2022-10-28
期刊：
影响因子：
15.1
通讯作者：
Peng, Li
中科院分区：
文献类型：
--
作者：
Peng, Jiang-Yun;Cai, Dian-Kui;Zeng, Ren-Li;Zhang, Chao-Yang;Li, Guan-Cheng;Chen, Si-Fan;Yuan, Xiao-Qing;Peng, Li
关键词：
Superenhancers drive abnormal gene expression in tumors and promote malignancy. However, the relationship between superenhancer‐associated long noncoding RNA (lncRNA) and abnormal metabolism is unknown. This study identifies a novel lncRNA, fatty acid synthesis‐related lncRNA (FASRL), whose expression is driven by upstream stimulatory factor 1 (USF1) through its superenhancer. FASRL promotes hepatocellular carcinoma (HCC) cell proliferation in vitro and in vivo. Furthermore, FASRL binds to acetyl‐CoA carboxylase 1 (ACACA), a fatty acid synthesis rate‐limiting enzyme, increasing fatty acid synthesis via the fatty acid metabolism pathway. Moreover, the expression of FASRL, USF1, and ACACA is increased, and their high expression indicates a worse prognosis in HCC patients. In summary, USF1 drives FASRL transcription via a superenhancer. FASRL binding to ACACA increases fatty acid synthesis and lipid accumulation to mechanistically exacerbate HCC. FASRL may serve as a novel prognostic marker and treatment target in HCC. This study identifies a novel lncRNA, fatty acid synthesis‐related lncRNA (FASRL), whose expression is driven by upstream stimulatory factor 1 through a superenhancer. FASRL binding to acetyl‐CoA carboxylase 1 increases fatty acid synthesis and lipid accumulation to mechanistically exacerbate hepatocellular carcinoma (HCC). FASRL serves as a novel potential prognostic marker and treatment target in HCC.
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