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
Oncogenejournal_title
Oncogeneauthors
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 Ldoi
10.1038/s41388-020-01417-6subject
Has Abstractpub_date
2020-09-01 00:00:00pages
6099-6112issue
38eissn
0950-9232issn
1476-5594pii
10.1038/s41388-020-01417-6journal_volume
39pub_type
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