Sodium butyrate enhances sorafenib-induced ferroptosis and immunogenic cell death by modulating IRF2-Oasl2-cGAS pathway in colorectal cancer.

ABSTRACT: While much attention has been focused on the direct cytotoxic effects of anticancer agents on tumor cells, emerging evidence suggests that the induction of immunogenic cell death (ICD) and the consequent remodeling of the tumor microenvironment may critically influence overall therapeutic efficacy. Sorafenib, a multitargeted tyrosine kinase inhibitor, can induce ferroptosis and thereby trigger ICD, offering the potential to overcome chemoresistance and coordinate systemic antitumor immunity. However, its therapeutic efficacy in colorectal cancer (CRC) remains limited, attributing to its low efficiency in inducing ICD. Herein, this study investigates combined sodium butyrate (NaB) and sorafenib in liposomal co-delivery system (LipNaB@Sor) at an optimal 1:1 M ratio in CRC. LipNaB@Sor synergi

SUBMITTER: Xiang Y 

PROVIDER: S-EPMC12639863 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature