ArticleMolecular biology of the cell2009
Role of the tumor suppressor PTEN in antioxidant responsive element-mediated transcription and associated histone modifications.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 93 citations in OpenAlex.
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- MiR-342-3p inhibits LCSC oncogenicity and cell stemness through HDAC7/PTEN axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- A PTEN variant uncouples longevity from impaired fitness in Caenorhabditis elegans with reduced insulin/IGF-1 signaling.Nature communications · 2021Article
- Insights into the Role of Oxidative Stress in Ovarian Cancer.Oxidative medicine and cellular longevity · 2021Review
- Asparaginyl endopeptidase (AEP) regulates myocardial apoptosis in response to radiation exposure via alterations in NRF2 activation.American journal of cancer research · 2021Article
- PTEN as a Guardian of the Genome: Pathways and Targets.Cold Spring Harbor perspectives in medicine · 2020Review
- Oxidative Stress in Cancer.Cancer cell · 2020Review
- Redox control of vascular biology.BioFactors (Oxford, England) · 2020Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Coordinated regulation of PI3-kinase (PI3K) and the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) plays a pivotal role in various cell functions. PTEN is deficient in many cancer cells, including Jurkat human leukemia. Here, we demonstrate that the status of PTEN determines cellular susceptibility to oxidative stress through antioxidant-responsive element (ARE)-mediated transcription of detoxification genes. We found that ferritin H transcription was robustly induced in tert-butylhydroquinone (t-BHQ)-treated Jurkat cells via an ARE, and it was due to PTEN deficiency. Chromatin immunoprecipitation assays revealed that p300/CREB-binding protein (CBP) histone acetyltransferases and Nrf2 recruitment to the ARE and Bach1 release were blocked by the PI3K inhibitor LY294002, along with the partial inhibition of Nrf2 nuclear accumulation. Furthermore, acetylations of histone H3 Lys9 and Lys18, and deacetylation of Lys14 were associated with the PI3K-dependent ARE activation. Consistently, PTEN restoration in Jurkat cells inhibited t-BHQ-mediated expression of ferritin H and another ARE-regulated gene NAD(P)H:quinone oxidoreductase 1. Conversely, PTEN knockdown in K562 cells enhanced the response to t-BHQ. The PTEN status under t-BHQ treatment affected hydrogen peroxide-mediated caspase-3 cleavage. The PI3K-dependent ferritin H induction was observed by treatment with other ARE-activating agents ethoxyquin and hemin. Collectively, the status of PTEN determines chromatin modifications leading to ARE activation.
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