Sodium butyrate inhibits colorectal cancer development by reducing M2 macrophage polarization and PD-L1 expression.

ABSTRACT: Short-chain fatty acids (SCFAs), produced by gut bacteria, are being recognized as an important form of anticancer therapy; however, their antitumor potency and underlying mechanisms remain unclear. Here, we used single-cell transcriptomics to identify the mechanism by which the SCFA sodium butyrate (NaB) inhibited the development of colorectal cancer (CRC) and explored new strategies for combining NaB with existing immunotherapies against CRC. An azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model of colitis and a macrophage-deficient subcutaneous tumor model were used to determine NaB effects on CRC. RNA-sequencing profiled CRC immune landscape changes following NaB treatment. The potential synergy between NaB and programmed death receptor ligand 1 (PD-L1) blockade was ex

SUBMITTER: Han B 

PROVIDER: S-EPMC12710303 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature