ArticleJournal of translational medicine2026
Asiaticoside enhances the antitumor efficacy of MSLN-targeted CAR-T cells in ovarian cancer.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Post-Translational Modifications in Cancer-Associated CD8⁺ T-Cell Exhaustion: Mechanisms and Therapeutic Opportunities.International journal of biological sciences · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundChimeric antigen receptor (CAR)-T cell therapy faces significant challenges in treating solid tumors, primarily due to the immunosuppressive tumor microenvironment (TME) and rapid T-cell exhaustion mediated by cytokines such as transforming growth factor-β (TGF-β). Developing strategies to remodel the TME and sustain T-cell function is critical. In this study, we investigated a pharmacological strategy using Asiaticoside (AC), a natural compound, as an adjuvant to enhance the efficacy of mesothelin (MSLN)-targeting CAR-T cells in ovarian cancer.
methodsWe engineered MSLN-specific CAR-T cells and evaluated their therapeutic efficacy in combination with AC using in vitro co-culture assays and in vivo xenograft models. Transcriptional changes were analyzed via RNA sequencing (RNA-seq), while the underlying molecular mechanism was investigated by focusing on the TGF-β/SMAD signaling axis. In vivo efficacy and safety were evaluated in NCG mice bearing subcutaneous or intraperitoneal metastatic SKOV-3-luc ovarian tumors, treated with the combination of CAR-T cells and AC.
resultsAC treatment significantly potentiated CAR-T cell cytotoxicity and reduced the expression of exhaustion markers (PD-1, TIM-3, and LAG-3) upon continuous antigen exposure. Mechanistically, AC functioned as an inhibitor of TGF-β signaling, effectively suppressing TGF-β1-induced phosphorylation of SMAD2/3. In mouse models, the combination of AC and CAR-T therapy exerted superior antitumor activity compared to CAR-T monotherapy, significantly suppressing tumor growth without inducing systemic toxicity or organ damage.
conclusionOur findings demonstrate that AC alleviates CAR-T cell exhaustion and antagonizes TGF-β-mediated immunosuppression. AC represents a promising, clinically translatable pharmacological adjuvant to overcome the bottlenecks of CAR-T cell therapy in solid tumors.
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