ArticlePloS one2012
p53 inactivation upregulates p73 expression through E2F-1 mediated transcription.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- TP53 Loss Elevates NF-κB-IFN-β-MHC-Ia Signaling to Promote NK Cell Resistance in Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CDK8 Inhibition Increases E2F1 Transcriptional Activity and Promotes STAT3-Dependent Suppression of Mcl-1 in Triple-Negative Breast Cancer Cell Line MDA-MB-468.International journal of molecular sciences · 2026Article
- Distinct Regulation of theCells · 2026Article
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- CENPE Inhibition Leads to Mitotic Catastrophe and DNA Damage in Medulloblastoma Cells.Cancers · 2021Article
- Article
- Review
- Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.International journal of molecular sciences · 2020Article
- Silencing E3 Ubiqutin ligase ITCH as a potential therapy to enhance chemotherapy efficacy in p53 mutant neuroblastoma cells.Scientific reports · 2020Article
- DMPK is a New Candidate Mediator of Tumor Suppressor p53-Dependent Cell Death.Molecules (Basel, Switzerland) · 2019Article
- Phenformin inhibits growth and epithelial-mesenchymal transition of ErbB2-overexpressing breast cancer cells through targeting the IGF1R pathway.Oncotarget · 2017Article
- p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells.PloS one · 2017Article
- miRNA-193a-5p repression of p73 controls Cisplatin chemoresistance in primary bone tumors.Oncotarget · 2016Article
- Dysfunctional telomeres induce p53-dependent and independent apoptosis to compromise cellular proliferation and inhibit tumor formation.Aging cell · 2016Article
- A Designed Inhibitor of p53 Aggregation Rescues p53 Tumor Suppression in Ovarian Carcinomas.Cancer cell · 2016Article
- Article
- Preclinical activity of combined HDAC and KDM1A inhibition in glioblastoma.Neuro-oncology · 2015Article
- TAp73 and ΔNp73 have opposing roles in 5-aza-2'-deoxycytidine-induced apoptosis in breast cancer cells.Molecules and cells · 2014Article
- Metformin selectively targets tumor-initiating cells in ErbB2-overexpressing breast cancer models.Cancer prevention research (Philadelphia, Pa.) · 2014Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While p73 overexpression has been associated with increased apoptosis in cancer tissues, p73 overexpressing tumors appear to be of high grade malignancy. Why this putative tumor suppressor is overexpressed in cancer cells and what the function of overexpressed p73 is in breast cancers are critical questions to be addressed. By investigating the effect of p53 inactivation on p73 expression, we found that both protein and mRNA levels of TAp73 were increased in MCF-7/p53siRNA cells, MCF-7/p53mt135 cells and HCT-116/p53-/- cells, as compared to wild type control, suggesting that p53 inactivation by various forms upregulates p73. We showed that p53 knockdown induced p73 was mainly regulated at the transcriptional level. However, although p53 has a putative binding site in the TAp73 promoter, deletion of this binding site did not affect p53 knockdown mediated activation of TAp73 promoter. Chromatin immuno-precipitation (ChIP) data demonstrated that loss of p53 results in enhanced occupancy of E2F-1 in the TAp73 promoter. The responsive sequence of p53 inactivation mediated p73 upregulation was mapped to the proximal promoter region of the TAp73 gene. To test the role of E2F-1 in p53 inactivation mediated regulation of p73 transcription, we found that p53 knockdown enhanced E2F-1 dependent p73 transcription, and mutations in E2F-1 binding sites in the TAp73 promoter abrogated p53 knockdown mediated activation of TAp73 promoter. Moreover, we demonstrated that p21 is a mediator of p53-E2F crosstalk in the regulation of p73 transcription. We concluded that p53 knockdown/inactivation may upregulate TAp73 expression through E2F-1 mediated transcriptional regulation. p53 inactivation mediated upregulation of p73 suggests an intrinsic rescuing mechanism in response to p53 mutation/inactivation. These findings support further analysis of the correlation between p53 status and p73 expression and its prognostic/predictive significance in human cancers.
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