Cited 11 times in

The interferon-inducible protein viperin controls cancer metabolic reprogramming to enhance cancer progression

Authors
 Kyung Mi Choi  ;  Jeong Jin Kim  ;  Jihye Yoo  ;  Ku Sul Kim  ;  Youngeun Gu  ;  John Eom  ;  Haengdueng Jeong  ;  Kyungeun Kim  ;  Ki Taek Nam  ;  Young Soo Park  ;  Joon-Yong Chung  ;  Jun-Young Seo 
Citation
 JOURNAL OF CLINICAL INVESTIGATION, Vol.132(24) : e157302, 2022-12 
Journal Title
JOURNAL OF CLINICAL INVESTIGATION
ISSN
 0021-9738 
Issue Date
2022-12
MeSH
Animals ; Glycolysis ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit / metabolism ; Interferons* / genetics ; Interferons* / metabolism ; Mice ; Neoplasms* / pathology ; Neoplastic Stem Cells / pathology ; Phosphatidylinositol 3-Kinases / metabolism ; Tumor Microenvironment
Keywords
Cancer ; Fatty acid oxidation ; Glucose metabolism ; Metabolism ; Oncology
Abstract
Metabolic reprogramming is an important cancer hallmark. However, the mechanisms driving metabolic phenotypes of cancer cells are unclear. Here, we show that the interferon-inducible (IFN-inducible) protein viperin drove metabolic alteration in cancer cells. Viperin expression was observed in various types of cancer and was inversely correlated with the survival rates of patients with gastric, lung, breast, renal, pancreatic, or brain cancer. By generating viperin knockdown or stably expressing cancer cells, we showed that viperin, but not a mutant lacking its iron-sulfur cluster-binding motif, increased lipogenesis and glycolysis via inhibition of fatty acid β-oxidation in cancer cells. In the tumor microenvironment, deficiency of fatty acids and oxygen as well as production of IFNs upregulated viperin expression via the PI3K/AKT/mTOR/HIF-1α and JAK/STAT pathways. Moreover, viperin was primarily expressed in cancer stem-like cells (CSCs) and functioned to promote metabolic reprogramming and enhance CSC properties, thereby facilitating tumor growth in xenograft mouse models. Collectively, our data indicate that viperin-mediated metabolic alteration drives the metabolic phenotype and progression of cancer.
Files in This Item:
T202300108.pdf Download
DOI
10.1172/JCI157302
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Nam, Ki Taek(남기택)
Seo, Jun Young(서준영) ORCID logo https://orcid.org/0000-0003-4004-2013
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/192910
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse

Links