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现在位置:首页 > 科研进展 > 最新重要论文(影响因子PNAS及以上)
ER-residential Nogo-B accelerates NAFLD-associated HCC mediated by metabolic reprogramming of oxLDL lipophagy, Nature Comm, 29 Jul 2019
2019-07-29 | 【     】【打印】【关闭

Nature Communications29 July, 2019,DOI:https://doi.org/10.1038/s41467-019-11274-x

ER-residential Nogo-B accelerates NAFLD-associated HCC mediated by metabolic reprogramming of oxLDL lipophagy

Yuan Tian, Bin Yang, Weinan Qiu, Yajing Hao, Zhenxing Zhang, Bo Yang, Nan Li, Shuqun Cheng, Zhangjun Lin, Yao-cheng Rui, Otto K. W. Cheung, Weiqin Yang, William K. K. Wu, Yue-Sun Cheung, Paul B. S. Lai, Jianjun Luo, Joseph J. Y. Sung, Runsheng Chen, Hong-Yang Wang, Alfred S. L. Cheng & Pengyuan Yang

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome that elevates the risk of hepatocellular carcinoma (HCC). Although alteration of lipid metabolism has been increasingly recognized as a hallmark of cancer cells, the deregulated metabolic modulation of HCC cells in the NAFLD progression remains obscure. Here, we discovers an endoplasmic reticulum-residential protein, Nogo-B, as a highly expressed metabolic modulator in both murine and human NAFLD-associated HCCs, which accelerates high-fat, high-carbohydrate diet-induced metabolic dysfunction and tumorigenicity. Mechanistically, CD36-mediated oxLDL uptake triggers CEBPβ expression to directly upregulate Nogo-B, which interacts with ATG5 to promote lipophagy leading to lysophosphatidic acid-enhanced YAP oncogenic activity. This CD36-Nogo-B-YAP pathway consequently reprograms oxLDL metabolism and induces carcinogenetic signaling for NAFLD-associated HCCs. Targeting the Nogo-B pathway may represent a therapeutic strategy for HCC arising from the metabolic syndrome.

文章链接:https://www.nature.com/articles/s41467-019-11274-x

相关报道:http://www.ibp.cas.cn/kyjz/zxdt/201907/t20190730_5353439.html

 

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