ArticleNature communications2025
Modulating the PPARγ pathway upregulates NECTIN4 and enhances chimeric antigen receptor (CAR) T cell therapy in bladder cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- PPARγ suppresses the tumorigenesis of retroperitoneal liposarcoma via inactivation of the PI3K/AKT signaling pathway.Journal of translational medicine · 2026Article
- Advancements in delivery systems for in vivo chimeric antigen receptor T-cell therapy in urological diseases.Current urology · 2026Review
- Targeting urological cancers with CAR-T cell therapy: current landscape and future directions.Journal of translational medicine · 2026Review
- Site-specific differences in Nectin-4 expression and associated immune contexture in advanced urothelial carcinoma: implications for Nectin-4-targeted ADCs.Therapeutic advances in medical oncology · 2026Article
- Recent advances in immunotherapy for bladder cancer: mechanisms, clinical applications, and future perspectives.Frontiers in oncology · 2026Review
- CD86 costimulation enhances the antitumor activity of NKG2D CAR-Macrophages and synergizes with Anti-PD-L1 therapy to suppress prostate cancer progression.Cell communication and signaling : CCS · 2025Article
- Evolving frontiers in bladder cancer immunotherapy: integrating BCG, immune checkpoints, viral vectors, nanotechnology, and CAR-based therapies.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
With the approval of the antibody-drug conjugate enfortumab vedotin (EV), NECTIN4 has emerged as a bona fide therapeutic target in urothelial carcinoma (UC). Here, we report the development of a NECTIN4-directed chimeric antigen receptor (CAR) T cell, which exhibits reactivity across cells expressing a range of endogenous NECTIN4, with enhanced activity in high expressors. We demonstrate that the PPARγ pathway, critical for luminal differentiation, transcriptionally controls NECTIN4, and that the PPARγ agonist rosiglitazone primes and augments NECTIN4 expression, thereby increasing sensitivity to NECTIN4-CAR T cell-mediated killing. NECTIN4-CAR T cells have potent anti-tumor activity even against EV resistant cells, which largely retain NECTIN4 expression, including in a post-EV biopsy cohort. Our results elucidate a therapeutically actionable mechanism that UC cells use to control NECTIN4 expression and suggest therapeutic approaches that leverage PPARγ agonists for rational combinations with NECTIN4-targeting agents in UC, as well as future potential treatment options for EV-refractory patients.
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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.