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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Published in | Molecules and cells Vol. 46; no. 8; pp. 473 - 475 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
United States
Korean Society for Molecular and Cellular Biology
31.08.2023
한국분자세포생물학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1016-8478 0219-1032 |
DOI | 10.14348/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 |
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ISSN: | 1016-8478 0219-1032 |
DOI: | 10.14348/molcells.2023.0094 |