Literature DB >> 30527495

Low DMT1 Expression Associates With Increased Oxidative Phosphorylation and Early Recurrence in Hepatocellular Carcinoma.

Toshifumi Hoki1, Eriko Katsuta2, Li Yan3, Kazuaki Takabe4, Fumito Ito5.   

Abstract

BACKGROUND: Despite a high rate of recurrences, long-term survival can be achieved after the resection of hepatocellular carcinoma (HCC) with effective local treatment. Discovery of adverse prognostic variables to identify patients with high risk of recurrence could improve the management of HCC. Accumulating evidence showing a link between carcinogenesis and increased expression of iron import proteins and intracellular iron prompted us to investigate a role of divalent metal-ion transporter-1 (DMT1) that binds and regulates a variety of divalent metals in HCC.
MATERIALS AND METHODS: Clinical and gene expression data from RNA seq in 369 HCC patients were obtained from The Cancer Genome Atlas. Disease-free survival was compared between DMT1 high- and low-expressing tumors, and gene set enrichment analysis was conducted.
RESULTS: Patients with lower expression of DMT1 exhibited significantly worse disease-free survival compared with the DMT1 high group (P = 0.044), notably in advanced-stage patients (P = 0.008). DMT1 expression did not differ in etiologies, stages, and differentiation status of HCC. Interestingly, DMT1 expression levels inversely associated with cellular respiratory function in HCC. Furthermore, gene set enrichment analysis revealed that metabolism-related gene sets such as glycolysis, oxidative phosphorylation, and reactive oxygen species pathway were significantly enriched in the DMT1 low-expressing HCC.
CONCLUSIONS: Low DMT1 expression associates with increased oxidative phosphorylation as well as glycolysis and identifies early recurrence in HCC patients after surgical treatment.
Copyright © 2018 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Divalent metal-ion transporter-1; Glycolysis; Hepatocellular carcinoma; Mitochondria; Oxidative phosphorylation; The Cancer Genome Atlas

Mesh:

Substances:

Year:  2019        PMID: 30527495      PMCID: PMC6291835          DOI: 10.1016/j.jss.2018.11.008

Source DB:  PubMed          Journal:  J Surg Res        ISSN: 0022-4804            Impact factor:   2.192


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