ArticleScience advances2023
The p23 co-chaperone is a succinate-activated COX-2 transcription factor in lung adenocarcinoma tumorigenesis.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- An Injectable Metal-Drug Supramolecular Condensate Enables Radiosensitization and Systemic Antitumor Immunity for Post-Surgical Osteosarcoma Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell and spatial transcriptomics reveal an arachidonic acid-related cellular atlas in lung adenocarcinoma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Nuclear prostaglandin E synthase 3 promotes hepatocellular carcinoma growth with immunosuppressive macrophage polarization via the SP1/TGF-β axis.Molecular biomedicine · 2026Article
- Succinylation: A Functional Nexus Between Metabolic Reprogramming and Epigenetic Modifications in Cancer.Molecules (Basel, Switzerland) · 2026Review
- Succinylation in cancer immunotherapy: mechanisms, biomarkers, and therapeutic implications.Frontiers in immunology · 2026Review
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Review
- P23 acts as a negative regulator of ferroptosis in NSCLC by blocking GPX4 degradation via chaperone-mediated autophagy.Molecular cancer · 2025Article
- Short-chain acyl post-translational modifications in cancers: Mechanisms, roles, and therapeutic implications.Cancer communications (London, England) · 2025Review
- Regulators of Cancer Progression: Succinylation.Cancers · 2025Review
- RBM14 enhances transcriptional activity of p23 regulating CXCL1 expression to induce lung cancer metastasis.Acta pharmaceutica Sinica. B · 2025Article
- p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke.International journal of molecular medicine · 2025Article
- Genome-wide association analysis and KASP markers development for protein quality traits in winter wheat.BMC plant biology · 2025Article
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- WWOX tuning of oleic acid signaling orchestrates immunosuppressive macrophage polarization and sensitizes hepatocellular carcinoma to immunotherapy.Journal for immunotherapy of cancer · 2024Article
- The integration of multidisciplinary approaches revealed PTGES3 as a novel drug target for breast cancer treatment.Journal of translational medicine · 2024Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
P23, historically known as a heat shock protein 90 (HSP90) co-chaperone, exerts some of its critical functions in an HSP90-independent manner, particularly when it translocates into the nucleus. The molecular nature underlying how this HSP90-independent p23 function is achieved remains as a biological mystery. Here, we found that p23 is a previously unidentified transcription factor of COX-2, and its nuclear localization predicts the poor clinical outcomes. Intratumor succinate promotes p23 succinylation at K7, K33, and K79, which drives its nuclear translocation for COX-2 transcription and consequently fascinates tumor growth. We then identified M16 as a potent p23 succinylation inhibitor from 1.6 million compounds through a combined virtual and biological screening. M16 inhibited p23 succinylation and nuclear translocation, attenuated COX-2 transcription in a p23-dependent manner, and markedly suppressed tumor growth. Therefore, our study defines p23 as a succinate-activated transcription factor in tumor progression and provides a rationale for inhibiting p23 succinylation as an anticancer chemotherapy.
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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.