ArticleThe Journal of biological chemistry2015
Mutant p53 promotes tumor cell malignancy by both positive and negative regulation of the transforming growth factor β (TGF-β) pathway.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- The miR-16-1-3p suppresses proliferation and invasiveness via the MDM2-p53 axis in TGF-β1 signaling in osteosarcoma.Molecular therapy. Oncology · 2026Article
- Growth resilience to weather variation in commercial free-ranging chickens in Ethiopia.BMC genomics · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Review
- Phenotypic targeting using magnetic nanoparticles for rapid characterization of cellular proliferation regulators.Science advances · 2024Article
- Article
- Asiaticoside delays senescence and attenuate generation of ROS in UV‑exposure cells through regulates TGF‑β1/Smad pathway.Experimental and therapeutic medicine · 2022Article
- Opposing Roles of Wild-type and Mutant p53 in the Process of Epithelial to Mesenchymal Transition.Frontiers in molecular biosciences · 2022Review
- Barriers to Immunotherapy in Ovarian Cancer: Metabolic, Genomic, and Immune Perturbations in the Tumour Microenvironment.Cancers · 2021Review
- Clinically Translatable Approaches of Inhibiting TGF-β to Target Cancer Stem Cells in TNBC.Biomedicines · 2021Review
- The Role of p53 Signaling in Colorectal Cancer.Cancers · 2021Review
- Ameliorative effects of colostrum against DMBA hepatotoxicity in rats.Saudi journal of biological sciences · 2021Article
- Senescence of Alveolar Type 2 Cells Drives Progressive Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021Article
- Review
- Th2 cells as an intermediate for the differentiation of naïve T cells into Th9 cells, associated with the Smad3/Smad4 and IRF4 pathway.Experimental and therapeutic medicine · 2020Article
- Gain-of-Function Mutations in p53 in Cancer Invasiveness and Metastasis.International journal of molecular sciences · 2020Review
- Mutant p53 Gain-of-Function: Role in Cancer Development, Progression, and Therapeutic Approaches.Frontiers in cell and developmental biology · 2020Review
- Mutant p53 on the Path to Metastasis.Trends in cancer · 2020Review
- Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis.International journal of molecular sciences · 2019Review
- Targeting the Oncogenic p53 Mutants in Colorectal Cancer and Other Solid Tumors.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Specific p53 mutations abrogate tumor-suppressive functions by gaining new abilities to promote tumorigenesis. Inactivation of p53 is known to distort TGF-β signaling, which paradoxically displays both tumor-suppressive and pro-oncogenic functions. The molecular mechanisms of how mutant p53 simultaneously antagonizes the tumor-suppressive and synergizes the tumor-promoting function of the TGF-β pathway remain elusive. Here we demonstrate that mutant p53 differentially regulates subsets of TGF-β target genes by enhanced binding to the MH2 domain in Smad3 upon the integration of ERK signaling, therefore disrupting Smad3/Smad4 complex formation. Silencing Smad2, inhibition of ERK, or introducing a phosphorylation-defective mutation at Ser-392 in p53 abrogates the R175H mutant p53-dependent regulation of these TGF-β target genes. Our study shows a mechanism to reconcile the seemingly contradictory observations that mutant p53 can both attenuate and cooperate with the TGF-β pathway to promote cancer cell malignancy in the same cell type.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.