ArticleCell death & disease2015
Mutant p53-R273H mediates cancer cell survival and anoikis resistance through AKT-dependent suppression of BCL2-modifying factor (BMF).
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 147 citations in OpenAlex.
- Mutant p53Molecular oncology · 2026Article
- Identification of Inflammatory Cell Death-Related Prognostic Signature and Its Regulatory Mechanism in Lung Adenocarcinoma.Cancer medicine · 2026Article
- p53-R280S mutation confers lenvatinib resistance in hepatocellular carcinoma via Bcl-2-mediated anti-apoptotic signaling.Molecular and cellular biochemistry · 2026Article
- A kinetically inert platinum antitumor agent overcomes mutant p53-driven chemoresistance via oxidative stress-mediated DNA damage.Medical oncology (Northwood, London, England) · 2026Article
- Apoptotic Signaling Across Breast Cancer Subtypes and Cryoablation-Induced Tissue Injury.International journal of molecular sciences · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Bcl-2 modifying factor (Bmf): "a mysterious stranger" in the Bcl-2 family proteins.Cell death and differentiation · 2026Review
- Molecular Basis of Simalikalactone D Sensitivity in Triple-Negative Breast Cancer Cells.Biomolecules · 2025Article
- Mutational Disruption of TP53: A Structural Approach to Understanding Chemoresistance.International journal of molecular sciences · 2025Article
- A base editing platform for the correction of cancer driver mutations unmasks conserved p53 transcription programs.Genome biology · 2025Article
- Charting the regulatory landscape of TP53 on transposable elements in cancer.Genome research · 2025Article
- Metabolic reprogramming and signaling adaptations in anoikis resistance: mechanisms and therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Article
- Coffee Wastes: A Sustainable Source of Natural Compounds Suppressing Colorectal Cancer Cell Viability.Oxidative medicine and cellular longevity · 2025Article
- Sodium arsenite-induced DNA methylation alterations exacerbated by p53 knockout in MCF7 cells.Heliyon · 2024Article
- miR-449a: A Promising Biomarker and Therapeutic Target in Cancer and Other Diseases.Cell biochemistry and biophysics · 2024Review
- Impact of microRNA variants on PI3K/AKT signaling in triple-negative breast cancer: comprehensive review.Medical oncology (Northwood, London, England) · 2024Review
- Advancements in precision nanomedicine design targeting the anoikis-platelet interface of circulating tumor cells.Acta pharmaceutica Sinica. B · 2024Review
- CCT6A promotes cell proliferation in colon cancer by targeting BIRC5 associated with p53 status.Cancer gene therapy · 2024Article
- Methylation-Based Characterization of a NewInternational journal of molecular sciences · 2024Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is the most frequently mutated tumor-suppressor gene in human cancers. Unlike other tumor-suppressor genes, p53 mutations mainly occur as missense mutations within the DNA-binding domain, leading to the expression of full-length mutant p53 protein. Mutant p53 proteins not only lose their tumor-suppressor function, but may also gain new oncogenic functions and promote tumorigenesis. Here, we showed that silencing of endogenous p53-R273H contact mutant, but not p53-R175H conformational mutant, reduced AKT phosphorylation, induced BCL2-modifying factor (BMF) expression, sensitized BIM dissociation from BCL-XL and induced mitochondria-dependent apoptosis in cancer cells. Importantly, cancer cells harboring endogenous p53-R273H mutant were also found to be inherently resistant to anoikis and lack BMF induction following culture in suspension. Underlying these activities is the ability of p53-R273H mutant to suppress BMF expression that is dependent on constitutively active PI3K/AKT signaling. Collectively, these findings suggest that p53-R273H can specifically drive AKT signaling and suppress BMF expression, resulting in enhanced cell survivability and anoikis resistance. These findings open the possibility that blocking of PI3K/AKT will have therapeutic benefit in mutant p53-R273H expressing cancers.
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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.