Tumor ABCC4-mediated release of PGE2 induces CD8⁺ T cell dysfunction and impairs PD-1 blockade in prostate cancer.

ABSTRACT: Prostate cancer presents as an immunologically "cold" malignancy, characterized by a lack of response to immunotherapy in the majority of patients. The dysfunction of prostate tumor metabolism is recognized as a critical factor in immune evasion, resulting in reduced effectiveness of immunotherapeutic interventions. Despite this awareness, the precise molecular mechanisms underpinning metabolic dysregulation in prostate cancer and its intricate relationship with immune evasion remain incompletely elucidated. In this study, we introduce the multi-drug resistance protein ABCC4/MRP4 as a key player prominently expressed in prostate cancer, exerting a pivotal role in suppressing the activity of intratumoral CD8⁺ T cells. Depletion of ABCC4 in prostate cancer cells halts the release

SUBMITTER: Li L 

PROVIDER: S-EPMC11380449 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature