Nuclear translocation of metabolic enzyme PKM2 participates in high glucose-promoted HCC metastasis by strengthening immunosuppressive environment

Bibliographic Details
Title: Nuclear translocation of metabolic enzyme PKM2 participates in high glucose-promoted HCC metastasis by strengthening immunosuppressive environment
Authors: Jiali Qian, Chuxin Huang, Mimi Wang, Ying Liu, Yingying Zhao, Miao Li, Xi Zhang, Xiangyu Gao, Yawen Zhang, Yi Wang, Jinya Huang, Jiajun Li, Qiwen Zhou, Rui Liu, Xuanchun Wang, Jiefeng Cui, Yehong Yang
Source: Redox Biology, Vol 71, Iss , Pp 103103- (2024)
Publisher Information: Elsevier, 2024.
Publication Year: 2024
Collection: LCC:Medicine (General)
LCC:Biology (General)
Subject Terms: Diabetes mellitus, Hepatocellular carcinoma, Pyruvate kinase M2, Thioredoxin, Chemerin, Medicine (General), R5-920, Biology (General), QH301-705.5
More Details: Although some cohort studies have indicated a close association between diabetes and HCC, the underlying mechanism about the contribution of diabetes to HCC progression remains largely unknown. In the study, we applied a novel HCC model in SD rat with diabetes and a series of high glucose-stimulated cell experiments to explore the effect of a high glucose environment on HCC metastasis and its relevant mechanism. Our results uncovered a novel regulatory mechanism by which nuclear translocation of metabolic enzyme PKM2 mediated high glucose-promoted HCC metastasis. Specifically, high glucose-increased PKM2 nuclear translocation downregulates chemerin expression through the redox protein TRX1, and then strengthens immunosuppressive environment to promote HCC metastasis. To the best of our knowledge, this is the first report to elucidate the great contribution of a high glucose environment to HCC metastasis from a new perspective of enhancing the immunosuppressive microenvironment. Simultaneously, this work also highlights a previously unidentified non-metabolic role of PKM2 and opens a novel avenue for cross research and intervention for individuals with HCC and comorbid diabetes.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2213-2317
Relation: http://www.sciencedirect.com/science/article/pii/S221323172400079X; https://doaj.org/toc/2213-2317
DOI: 10.1016/j.redox.2024.103103
Access URL: https://doaj.org/article/dd7690893a4940ccbc57103cb042a6de
Accession Number: edsdoj.7690893a4940ccbc57103cb042a6de
Database: Directory of Open Access Journals
More Details
ISSN:22132317
DOI:10.1016/j.redox.2024.103103
Published in:Redox Biology
Language:English