BET inhibition induces GDH1-dependent glutamine metabolic remodeling and vulnerability in liver cancer
Life Metabolism, ISSN: 2755-0230, Vol: 3, Issue: 4, Page: loae016
2024
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Most Recent News
Fudan University Researcher Discusses Findings in Liver Cancer (BET inhibition induces GDH1-dependent glutamine metabolic remodeling and vulnerability in liver cancer)
2024 MAY 10 (NewsRx) -- By a News Reporter-Staff News Editor at NewsRx Drug Daily -- Fresh data on liver cancer are presented in a
Article Description
Bromodomain and extra-terminal domain (BET) proteins, which function partly through MYC proto-oncogene (MYC), are critical epigenetic readers and emerging therapeutic targets in cancer. Whether and how BET inhibition simultaneously induces metabolic remodeling in cancer cells remains unclear. Here we find that even transient BET inhibition by JQ-1 and other pan-BET inhibitors (pan-BETis) blunts liver cancer cell proliferation and tumor growth. BET inhibition decreases glycolytic gene expression but enhances mitochondrial glucose and glutamine oxidative metabolism revealed by metabolomics and isotope labeling analysis. Specifically, BET inhibition downregulates miR-30a to upregulate glutamate dehydrogenase 1 (GDH1) independent of MYC, which produces α-ketoglutarate for mitochondrial oxidative phosphorylation (OXPHOS). Targeting GDH1 or OXPHOS is synthetic lethal to BET inhibition, and combined BET and OXPHOS inhibition therapeutically prevents liver tumor growth in vitro and in vivo. Together, we uncover an important epigenetic-metabolic crosstalk whereby BET inhibition induces MYC-independent and GDH1-dependent glutamine metabolic remodeling that can be exploited for innovative combination therapy of liver cancer.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85195492799&origin=inward; http://dx.doi.org/10.1093/lifemeta/loae016; http://www.ncbi.nlm.nih.gov/pubmed/39872506; https://academic.oup.com/lifemeta/article/doi/10.1093/lifemeta/loae016/7658715; https://dx.doi.org/10.1093/lifemeta/loae016; https://academic.oup.com/lifemeta/article/3/4/loae016/7658715
Oxford University Press (OUP)
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