ArticleOncogene2011
p53 promotes cellular survival in a context-dependent manner by directly inducing the expression of haeme-oxygenase-1.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Navigating heme pathways: the breach of heme oxygenase and hemin in breast cancer.Molecular and cellular biochemistry · 2025Review
- Multicellular model of neuroblastoma proposes unconventional therapy based on multiple roles of p53.PLoS computational biology · 2024Article
- A non-canonical role of ELN protects from cellular senescence by limiting iron-dependent regulation of gene expression.Redox biology · 2024Article
- Endothelin-1 as a Mediator of Heme Oxygenase-1-Induced Stemness in Colorectal Cancer: Influence of p53.Journal of personalized medicine · 2021Article
- Review
- Article
- Redox Potential of Antioxidants in Cancer Progression and Prevention.Antioxidants (Basel, Switzerland) · 2020Review
- Heme Oxygenase-1 in Central Nervous System Malignancies.Journal of clinical medicine · 2020Review
- Article
- Article
- Drosophila p53 integrates the antagonism between autophagy and apoptosis in response to stress.Autophagy · 2019Article
- Decreased Expression of SRSF2 Splicing Factor Inhibits Apoptotic Pathways in Renal Cancer.International journal of molecular sciences · 2016Article
- Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy.Oxidative medicine and cellular longevity · 2016Review
- Modulation of Melanogenesis by Heme Oxygenase-1 via p53 in Normal Human Melanocytes.Chonnam medical journal · 2016Article
- Renal iron overload in rats with diabetic nephropathy.Physiological reports · 2015Article
- Nuclear cytoplasmic trafficking of proteins is a major response of human fibroblasts to oxidative stress.Journal of proteome research · 2014Article
- Subcellular proteomics reveals a role for nucleo-cytoplasmic trafficking at the DNA replication origin activation checkpoint.Journal of proteome research · 2013Article
- Metabolic regulation of oxygen and redox homeostasis by p53: lessons from evolutionary biology?Free radical biology & medicine · 2012Review
- Lack of p53 decreases basal oxidative stress levels in the brain through upregulation of thioredoxin-1, biliverdin reductase-A, manganese superoxide dismutase, and nuclear factor kappa-B.Antioxidants & redox signaling · 2012Article
- Bilirubin inhibits neointima formation and vascular smooth muscle cell proliferation and migration.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A variety of cellular insults activate the tumour suppressor p53, leading generally to cell-cycle arrest or apoptosis. However, it is not inconceivable that cellular protective mechanisms may be required to keep cells alive while cell-fate decisions are made. In this respect, p53 has been suggested to perform functions that allow cells to survive, by halting of the cell-cycle, and thus preventing immediate cell death. Nonetheless, the existence of direct pro-survival p53 target genes regulating cellular survival is lacking. We show here evidence for p53-dependent cellular survival in a context-dependent manner. Both mouse and human cells lacking p53 are hypersensitive to hydrogen peroxide (H(2)O(2))-induced cell death compared with their isogenic wild-type counterparts. By contrast, p53(-/-) cells are expectedly resistant to cell death upon exposure to DNA-damaging agents such as cisplatin (CDDP) and etoposide. Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner. Consistently, p53, but not its homologue p73, activated HO-1 expression and was bound to the HO-1 promoter specifically only upon H(2)O(2) treatment. Moreover, silencing HO-1 expression enhanced cell death upon H(2)O(2) treatment only in p53-proficient cells. Finally, H(2)O(2)-mediated cell death was rescued significantly in p53-deficient cells by antioxidant treatment, as well as by bilirubin, a by-product of HO-1 metabolism. Taken together, these data demonstrate a direct role for p53 in promoting cellular survival in a context-specific manner through the activation of a direct transcriptional target, HO-1.
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