RIPK3 Activation Induces TRIM28 Derepression in Cancer Cells and Enhances the Anti-tumor Microenvironment

We identified TRIM28 as a co-repressor that regulates transcriptional activity during necroptosis. RIPK3 activation induces TRIM28 phosphorylation at serine 473, inhibiting its chromatin binding activity, thereby contributing to the transactivation of NF-?B and other transcription factors, such as SOX9. This leads to elevated cytokine expression, which then potentiates immunoregulatory processes, such as DC maturation. The expression of RIPK3 has a significant positive association with the tumor-infiltrating immune cells populations in various tumor type, thereby activating anti-cancer responses. Overall design: ChIP-seq of HT29 cells as described