ArticleCell reports2022
Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome.Nature communications · 2025Article
- The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025Review
- Deletion of p63 exon 13 in mice reveals C-terminal isoform-specific functions in epithelial development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- Alternative splicing in the DBD linker region of p63 modulates binding to DNA and iASPP in vitro.Cell death & disease · 2025Article
- Cardiocutaneous syndrome is caused by aggregation of iASPP mutants.Cell death discovery · 2024Article
- Primary and Orthotopic Murine Models of Nasopharyngeal Carcinoma Reveal Molecular Mechanisms Underlying its Malignant Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- PANX1-mediated ATP release confers FAM3A's suppression effects on hepatic gluconeogenesis and lipogenesis.Military Medical Research · 2024Article
- Ubiquitination plays an important role during the formation of chicken primordial germ cells.Journal of animal science · 2024Article
- p53 inhibitor iASPP is an unexpected suppressor of KRAS and inflammation-driven pancreatic cancer.Cell death and differentiation · 2023Article
- Regulation of immunological tolerance by the p53-inhibitor iASPP.Cell death & disease · 2023Article
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Concurrent mutation of a RAS oncogene and the tumor suppressor p53 is common in tumorigenesis, and inflammation can promote RAS-driven tumorigenesis without the need to mutate p53. Here, we show, using a well-established mutant RAS and an inflammation-driven mouse skin tumor model, that loss of the p53 inhibitor iASPP facilitates tumorigenesis. Specifically, iASPP regulates expression of a subset of p63 and AP1 targets, including genes involved in skin differentiation and inflammation, suggesting that loss of iASPP in keratinocytes supports a tumor-promoting inflammatory microenvironment. Mechanistically, JNK-mediated phosphorylation regulates iASPP function and inhibits iASPP binding with AP1 components, such as JUND, via PXXP/SH3 domain-mediated interaction. Our results uncover a JNK-iASPP-AP1 regulatory axis that is crucial for tissue homeostasis. We show that iASPP is a tumor suppressor and an AP1 coregulator.
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