ArticleNature communications2024
PJA1-mediated suppression of pyroptosis as a driver of docetaxel resistance in nasopharyngeal carcinoma.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- mTORC2 Phosphorylation of GSDME-N Drives Cullin4B-Mediated Proteasomal Degradation to Suppress Pyroptosis and Confer Radioresistance in Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Biomimetic Copper-Caffeic Acid Nanozyme Activates Cuproptosis and Pyroptosis by Mimicking the Neutrophil Enzymatic Cascade.Advanced healthcare materials · 2026Article
- Review
- MYBL2 impedes cisplatin sensitivity through suppressing GSDME-mediated pyroptosis in lung adenocarcinoma.Cell death discovery · 2026Article
- BIRC6 prevents GSDME-mediated pyroptosis and promotes cisplatin resistance via a non-canonical UBC domain-dependent steric hindrance.Cell communication and signaling : CCS · 2026Article
- Decoding the crosstalk between ubiquitination and other post-translational modifications in cancer immunity: from mechanisms to clinical prospects.NPJ precision oncology · 2026Review
- The dual role of pyroptosis in prostate cancer: new perspectives from molecular mechanisms to clinical translation.Molecular biology reports · 2026Review
- Fusobacterium nucleatum manipulates host autophagy to promote its intracellular survival and treatment resistance in nasopharyngeal carcinoma.Molecular cancer · 2026Article
- PTM-Related Signatures Predict Lymph Node Metastasis and Shape Microenvironment in Hepatocellular Carcinoma: A Single-Cell and Bulk Integrated Analysis.Journal of hepatocellular carcinoma · 2026Article
- LC3-dependent intercellular transfer of phosphorylated STAT1/2 elicits CXCL9+ macrophages and enhances radiation-induced antitumor immunity.The Journal of clinical investigation · 2025Article
- Vinburnine Sensitizes Radiotherapy Efficacy in Nasopharyngeal Carcinoma by Triggering Pyroptosis and Immune Responses via Activation of EDAR-NFκB Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cinobufagin loaded Prussian blue-like nanoparticles for chemo/gas therapy of multidrug resistant cancer.Journal of nanobiotechnology · 2025Article
- Targeting Methylglyoxal Metabolism to Enhance Ferroptosis Sensitivity in Tumor Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- 5-ALA mediated PDT induces pyroptosis in colorectal cancer cells by targeting the caspase-1/GSDMD pathway.Lasers in medical science · 2025Article
- Degradation of IRF6 by TRIM59 in tumor cells triggers PGM1-mediated glycolysis to regulate cell proliferation in neuroblastoma.Cell death & disease · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Antitumor/anti-inflammatory effects/tissue healing as an all-in-one therapeutic strategy for nasopharyngeal carcinoma.Journal of nanobiotechnology · 2025Article
- Tissue-resident microbiota signature in nasopharyngeal carcinoma.Microbiome · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Chemoresistance is a main reason for treatment failure in patients with nasopharyngeal carcinoma, but the exact regulatory mechanism underlying chemoresistance in nasopharyngeal carcinoma remains to be elucidated. Here, we identify PJA1 as a key E3 ubiquitin ligase involved in nasopharyngeal carcinoma chemoresistance that is highly expressed in nasopharyngeal carcinoma patients with nonresponse to docetaxel-cisplatin-5-fluorouracil induction chemotherapy. We find that PJA1 facilitates docetaxel resistance by inhibiting GSDME-mediated pyroptosis in nasopharyngeal carcinoma cells. Mechanistically, PJA1 promotes the degradation of the mitochondrial protein PGAM5 by increasing its K48-linked ubiquitination at K88, which further facilitates DRP1 phosphorylation at S637 and reduced mitochondrial reactive oxygen species production, resulting in suppression of GSDME-mediated pyroptosis and the antitumour immune response. PGAM5 knockdown fully restores the docetaxel sensitization effect of PJA1 knockdown. Moreover, pharmacological targeting of PJA1 with the small molecule inhibitor RTA402 enhances the docetaxel sensitivity of nasopharyngeal carcinoma in vitro and in vivo. Clinically, high PJA1 expression indicates inferior survival and poor clinical efficacy of TPF IC in nasopharyngeal carcinoma patients. Our study emphasizes the essential role of E3 ligases in regulating chemoresistance and provides therapeutic strategies for nasopharyngeal carcinoma based on targeting the ubiquitin-proteasome system.
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