NADH-Reductive Stress in Cancer Cell Proliferation

NRF2-mediated ALDH3A1 upregulation via pharmacologic inhibition or KEAP1 mutation induces NADH-reductive stress. The disruption of mitochondrial Complex I activity leads to metabolic vulnerability in Keap1-dependent and mutant cell lines, increasing NADH levels. The induction of NADH-reductive stres...

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Bibliographic Details
Published inMolecules and cells Vol. 46; no. 8; pp. 473 - 475
Main Author Choi, Dahee
Format Journal Article
LanguageEnglish
Published United States Korean Society for Molecular and Cellular Biology 31.08.2023
한국분자세포생물학회
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ISSN1016-8478
0219-1032
DOI10.14348/molcells.2023.0094

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Summary:NRF2-mediated ALDH3A1 upregulation via pharmacologic inhibition or KEAP1 mutation induces NADH-reductive stress. The disruption of mitochondrial Complex I activity leads to metabolic vulnerability in Keap1-dependent and mutant cell lines, increasing NADH levels. The induction of NADH-reductive stress selectively blocks the proliferation of cancer cell lines. NRF2, nuclear factor erythroid-derived 2-related factor 2; KEAP1, Kelch-like ECH-associated protein 1; ALDH3A1, aldehyde dehydrogenase 3 family member A1; NADH, nicotinamide adenine dinucleotide hydride; TCA, tricarboxylic acid; OXPHOS, oxidative phosphorylation. KCI Citation Count: 0
ISSN:1016-8478
0219-1032
DOI:10.14348/molcells.2023.0094