Targeting SRSF1 improves cancer immunotherapy by dually acting on CD8⁺T and tumor cells.

ABSTRACT: Serine arginine-rich splicing factor 1 (SRSF1) is a key oncogenic splicing factor in various cancers, promoting abnormal gene expression through post-translational regulation. Although the protumoral function of SRSF1 is well-established, the effects of inhibiting tumor-intrinsic SRSF1 on the tumor microenvironment and its impact on CD8⁺ T cell-mediated antitumor immunity remain unclear. Our findings indicate that depleting SRSF1 in CD8⁺ T cells improve antitumor immune function, glycolytic metabolism, and the efficacy of adoptive T cell therapy. The inactivation of SRSF1 in tumor cells reduces transcription factors, including c-Jun, c-myc, and JunB, facilitating glycolytic metabolism reprogramming, which restores CD8⁺ T cell function and inhibits tumor gro

SUBMITTER: Zhu GQ 

PROVIDER: S-EPMC11751439 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature