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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Tian Y,Yang B,Qiu W,Hao Y,Zhang Z,Yang B,Li N,Cheng S,Lin Z,Rui YC,Cheung OKW,Yang W,Wu WKK,Cheung YS,Lai PBS,Luo J,Sung JJY,Chen R,Wang HY,Cheng ASL,Yang P

doi

10.1038/s41467-019-11274-x

subject

Has Abstract

pub_date

2019-07-29 00:00:00

pages

3391

issue

1

issn

2041-1723

pii

10.1038/s41467-019-11274-x

journal_volume

10

pub_type

杂志文章

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