ArticleEMBO molecular medicine2016
Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients.
Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.
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Who cites it
102 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.
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- Assessing the significance of CCNE1 overexpression in triple negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
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- MCD enzyme deficiency drives early mortality and multiorgan metabolic disruption in Dahl salt-sensitive rats.iScience · 2026Article
- Prospective Breast Cancer Biomarkers Identified Using miR-526b-Driven Metabolic Alterations.Cancer informatics · 2026Article
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- Knockdown of NDUFAF6 inhibits breast cancer progression via promoting mitophagy and apoptosis.Cancer biology & therapy · 2025Article
- Genomic data mining reveals hub genes and lncRNAs as prognostic biomarkers in breast cancer.Scientific reports · 2025Article
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- Volatile Organic Compounds in Teas: Identification, Extraction, Analysis, and Application of Tea Aroma.Foods (Basel, Switzerland) · 2025Review
- UNC93B1: a novel immune-related prognostic biomarker in breast cancer.Discover oncology · 2025Article
- Single-cell analysis of gene regulatory networks in the mammary glands of P4HA1-knockout mice.PLoS genetics · 2025Article
42 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-cancer drugs often increase reactive oxygen species (ROS) and cause DNA damage. Here, we highlight a new cross talk between chronic oxidative stress and the histone variant H2AX, a key player in DNA repair. We observe that persistent accumulation of ROS, due to a deficient JunD-/Nrf2-antioxidant response, reduces H2AX protein levels. This effect is mediated by an enhanced interaction of H2AX with the E3 ubiquitin ligase RNF168, which is associated with H2AX poly-ubiquitination and promotes its degradation by the proteasome. ROS-mediated H2AX decrease plays a crucial role in chemosensitivity. Indeed, cycles of chemotherapy that sustainably increase ROS reduce H2AX protein levels in Triple-Negative breast cancer (TNBC) patients. H2AX decrease by such treatment is associated with an impaired NRF2-antioxidant response and is indicative of the therapeutic efficiency and survival of TNBC patients. Thus, our data describe a novel ROS-mediated regulation of H2AX turnover, which provides new insights into genetic instability and treatment efficacy in TNBC patients.
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