A novel mitochondrial amidoxime reducing component 2 is a favorable indicator of cancer and suppresses the progression of hepatocellular carcinoma by regulating the expression of p27.

Abstract:

:Hepatocellular carcinoma (HCC) is the fifth leading cause of cancer-related mortality in the United States. Exploring the mechanism of HCC and identifying ideal targets is critical. In the present study, we demonstrated metabolism dysfunction might be a key diver for the development of HCC. The mitochondrial amidoxime reducing component 2 (MARC2) as a newly discovered molybdenum enzyme was downregulated in human HCC tissues and HCC cells. Downregulated MARC2 was significantly associated with clinicopathological characteristics of HCC, such as tumor size, AFP levels, and tumor grade and was an independent risk factor of poor prognosis. Both in vitro and in vivo studies suggested that MARC2 suppressed the progression of HCC by regulating the protein expression level of p27. The Hippo signaling pathway and RNF123 were required for this process. Moreover, MARC2 regulated expression of HNF4A via the Hippo signaling pathway. HNF4A was recruited to the promoter of MARC2 forming a feedback loop. MARC2 levels were downregulated by methylation. We demonstrated the prognostic value of MARC2 in HCC and determined the mechanism by which MARC2 suppressed the progression of HCC in this study. These findings may lead to new therapeutic targets for HCC.

journal_name

Oncogene

journal_title

Oncogene

authors

Wu D,Wang Y,Yang G,Zhang S,Liu Y,Zhou S,Guo H,Liang S,Cui Y,Zhang B,Ma K,Zhang C,Liu Y,Sun L,Wang J,Liu L

doi

10.1038/s41388-020-01417-6

subject

Has Abstract

pub_date

2020-09-01 00:00:00

pages

6099-6112

issue

38

eissn

0950-9232

issn

1476-5594

pii

10.1038/s41388-020-01417-6

journal_volume

39

pub_type

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