ArticleCell death & disease2025
PLA2G7 promotes immune evasion of bladder cancer through the JAK-STAT-PDL1 axis.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Genomics/Genetics of Primary Biliary Cholangitis: The Case for a Functional SNP rs10893900 in ETS1/FLI1 and Review of the Literature.Clinical reviews in allergy & immunology · 2025Pooled it
- Sprayable hydrogel loaded with engineered fusion cellular vesicles for cancer recurrence suppression.Journal of nanobiotechnology · 2026Article
- ETS1 Orchestrates a Hybrid EMT Program Driving Metastasis and Immune Evasion.Cancer research · 2026Article
- Potential of RAD51C as a hub gene and therapeutic target in bladder cancer: insights from bioinformatics and experimental analysis.International journal of surgery (London, England) · 2026Article
- Tumor-intrinsic metabolic pathways essential for tumorigenesis and resistance to anti-PD1 in oncogenic Kras-driven lung adenocarcinoma.Cancer & metabolism · 2026Article
- Targeting PLA2G7 ameliorates high-fat diet-induced pulmonary injury in obese mice, uncovering a key mechanistic link to obesity-associated COPD.Respiratory research · 2026Article
- Cordyceps sinensis enhances the efficacy of anti-PD-1 immunotherapy in Lewis lung adenocarcinoma.Scientific reports · 2026Article
- The role of plectin as a druggable target in papillary thyroid carcinoma: therapeutic potential of troglitazone.Frontiers in immunology · 2026Article
- Mechanistic Insights into Maxing Shigan Decoction in Community-Acquired Pneumonia Based on Bioinformatics and Experimental Validation.Infection and drug resistance · 2026Article
- Targeted Nanoparticles for PROTAC-Mediated JAK1/JAK2 Degradation for Bladder Cancer Treatment.International journal of nanomedicine · 2026Article
- Mechanisms of microbiome-immune interactions in bladder cancer and targeted regulatory strategies.Frontiers in immunology · 2026Review
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- Lipoprotein-associated phospholipase A2 (Lp-PLA2): a key hub linking lipid metabolism and immune inflammation.Frontiers in immunology · 2026Review
- ERO1A promotes the proliferation, migration and invasion of bladder cancer through ALOX5 mediated activation of JAK-STAT signaling pathway.Journal of translational medicine · 2025Article
- Persistent myeloid cell reprogramming despite miltefosine treatment in leishmania-infected macaques.iScience · 2025Article
- Multi-omics exploration demonstrated the antidepressant effects of chrysophanol on diabetes-depression comorbidity rats via inflammatory, and neurodegenerative axes.Scientific reports · 2025Article
- Assessment of the Significance of LP-PLA2, DPYSL2, and 8-OHdG in the Oncological Diagnosis of Patients with Brain Tumors and Vitamin D Deficiency.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Targeting immune checkpoints such as Programmed death ligand-1 (PD-L1) and Programmed cell death 1 (PD-1) has been approved for treating bladder cancer and shows promising clinical benefits. However, the relatively low response rate highlights the need to seek an alternative strategy to traditional PD-1/PD-L1 targeting immunotherapy. In this study, we found that PLA2G7 is significantly elevated in bladder cancer and correlates with worse prognosis. In vitro experiments demonstrated that knockdown of PLA2G7 does not significantly affect the proliferation, migration, and invasion of bladder cancer cells. Flow cytometry detection, as well as protein and RNA detection, showed that knockdown of PLA2G7 significantly inhibits PD-L1 expression and suppresses the growth of transplanted tumors by promoting CD8 + T-cell infiltration. Further experiments showed that PLA2G7 regulates the JAK-STAT pathway to promote PD-L1 expression by upregulating the phosphorylation of STAT1 and STAT3. Meanwhile, results from syngeneic mouse models indicated that PLA2G7 suppression and anti-CTLA4 therapy have synergistic effects on tumor burden and mouse survival. In addition, we found that ETS1 promotes PLA2G7 overexpression in bladder cancer cells. In summary, our findings provide a novel immunotherapeutic strategy against bladder cancer through targeting the ETS1-PLA2G7-STAT1/STAT3-PD-L1 axis.
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