ArticleToxicology letters2015
Deregulation of NR2E3, an orphan nuclear receptor, by benzo(a)pyrene-induced oxidative stress is associated with histone modification status change of the estrogen receptor gene promoter.
Article in Toxicology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review.Mutation research. Reviews in mutation researchPooled it
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β-catenin Signaling via Epigenetic Dysregulation that Enhances Sp1-β catenin-p300 Interactions in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Regulation of the stem‑like properties of estrogen receptor‑positive breast cancer cells through NR2E3/NR2C2 signaling.Experimental and therapeutic medicine · 2023Article
- Biliverdin regulates NR2E3 and zebrafish retinal photoreceptor development.Scientific reports · 2022Article
- Polycyclic Aromatic Hydrocarbons and Mammary Cancer Risk: Does Obesity Matter too?Journal of cancer immunology · 2021Article
- Role of Nkx2.5 in HCell stress & chaperones · 2019Article
- NR2E3 is a key component in p53 activation by regulating a long noncoding RNA DINO in acute liver injuries.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Loss of NR2E3 represses AHR by LSD1 reprogramming, is associated with poor prognosis in liver cancer.Scientific reports · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that NR2E3, an orphan nuclear receptor, plays an important role in maintaining the basal expression of estrogen receptor α (ER) and that the NR2E3 level is highly correlated with the relapse-free survival of breast cancer patients. Here, we investigated the role of NR2E3 in benzo(a)pyrene (BaP)-mediated cell injury. BaP treatment reduced NR2E3 homo-dimer formation and expression and subsequently decreased ER expression. The chromatin immunoprecipitation assay results showed that the treatment of MCF-7 breast cancer cells and the mouse liver with BaP released NR2E3 from the ER promoter to transform the transcriptionally active histone modification status into a repressive state. NR2E3 depletion in MCF-7 cells also induced a similar inactive epigenetic status in the ER promoter region, indicating that NR2E3 is an essential epigenetic player that maintains basal ER expression. Interestingly, these negative effects of BaP on the expression levels of NR2E3 and ER were rescued by antioxidant treatment. Collectively, our study provides novel evidence to show that BaP-induced oxidative stress decreases ER expression, in part by regulating NR2E3 function, which modulates the epigenetic status of the ER promoter. NR2E3 is likely an essential epigenetic player that maintains basal ER expression to protect cells from BaP-induced oxidative injury.
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