ArticleProceedings of the National Academy of Sciences of the United States of America2022
Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. 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, 25 citations in OpenAlex.
- DNA-contact mutant p53 displaces BRCA2 from chromatin and drives R-loop-associated genome instability.Genome biology · 2026Article
- Tridax procumbens promotes apoptosis and suppresses markers of proliferation, growth, and metastasis in pancreatic ductal adenocarcinoma cells.BMC complementary medicine and therapies · 2026Article
- Proteasomal proteolysis in p62 condensates directs tumor suppression or growth depending on their subcellular localization.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- CircTP53/USP10/p53 signaling Axis as a Novel Regulator of Progression and Prognosis of Head and Neck Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sensitizing Immune-Refractory Ovarian Tumors via p53 Mutation-Tailored Immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- Bibliometric analysis and visualization of Connexin 43 in the field of solid tumor research(2000-2024).Frontiers in immunology · 2025Article
- Epigenetic modulation of human neurobiological disorders: Lesch-Nyhan disease as a model disorder.AIMS neuroscience · 2025Review
- p53 Genetics and Biology in Lung Carcinomas: Insights, Implications and Clinical Applications.Biomedicines · 2024Review
- Proximity labeling reveals dynamic changes in the SQSTM1 protein network.bioRxiv : the preprint server for biology · 2024Article
- APR-246 as a radiosensitization strategy for mutant p53 cancers treated with alpha-particles-based radiotherapy.Cell death & disease · 2024Article
- Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability.Molecular systems biology · 2024Article
- Recent Advances on Mutant p53: Unveiling Novel Oncogenic Roles, Degradation Pathways, and Therapeutic Interventions.Biomolecules · 2024Review
- Differential effect of plakoglobin in restoring the tumor suppressor activities of p53-R273H vs. p53-R175H mutants.PloS one · 2024Article
- p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Different Roles of Apoptosis and Autophagy in the Development of Human Colorectal Cancer.International journal of molecular sciences · 2023Review
- Anticancer efficacy of hirsuteine against colorectal cancer by opposite modulation of wild-type and mutant p53.Discover oncology · 2023Article
- Novel Susceptibility Genes Drive Familial Non-Medullary Thyroid Cancer in a Large Consanguineous Kindred.International journal of molecular sciences · 2023Article
- The ubiquitin ligase TRIM21 regulates mutant p53 accumulation and gain of function in cancer.The Journal of clinical investigation · 2023Article
- Hypoxia-induced long non-coding RNA LINC00460 promotes p53 mediated proliferation and metastasis of pancreatic cancer by regulating the miR-4689/UBE2V1 axis and sequestering USP10.International journal of medical sciences · 2023Article
Corrections and comments
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Authors and funding
21 authors at 4 institutions in 3 countries.
Funding
Abstract
Missense mutations in the p53 tumor suppressor abound in human cancer. Common (“hotspot”) mutations endow mutant p53 (mutp53) proteins with oncogenic gain of function (GOF), including enhanced cell migration and invasiveness, favoring cancer progression. GOF is usually attributed to transcriptional effects of mutp53. To elucidate transcription-independent effects of mutp53, we characterized the protein interactome of the p53R273H mutant in cells derived from pancreatic ductal adenocarcinoma (PDAC), where p53R273H is the most frequent p53 mutant. We now report that p53R273H, but not the p53R175H hotspot mutant, interacts with SQSTM1/p62 and promotes cancer cell migration and invasion in a p62-dependent manner. Mechanistically, the p53R273H-p62 axis drives the proteasomal degradation of several cell junction–associated proteins, including the gap junction protein Connexin 43, facilitating scattered cell migration. Concordantly, down-regulation of Connexin 43 augments PDAC cell migration, while its forced overexpression blunts the promigratory effect of the p53R273H-p62 axis. These findings define a mechanism of mutp53 GOF.
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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.