c-Myb controls inflammatory circuit in breast cancer via NF-kB suppression



Year of publication 2018
Type Conference abstract
Description Inflammatory responses play decisive roles at different stages of tumor development. Inflammatory mediators such as cytokines and chemokines may directly increase vascular permeability, promote the survival of circulating metastatic seeds or engage immune cells to assist the escape and proliferation at the secondary site. Our recent results indicate that transcription factor c-Myb acts as repressor of a subset of inflammatory genes in ER-negative BCs. We presume that these specific immune response genes might be critical for BC dissemination. We aim to investigate how the transcriptional module induced by c-Myb in BC cells encodes functional programs of the inflammatory response. We focused on NF-kB transcription factor family as i) in silico analysis showed that the most over-represented TF-binding sites within the inflammatory gene set were NF-kB family motifs; ii) several NF-kB target genes are down-regulated in Myb-overexpressing 4T1 and E0771 cells; and iii) MYB expression and constitutive NF-kB activity are inversely correlated in human BC cell lines. We found that c-Myb reduced NF-kB transactivation as determined by luciferase reporter assay and NF-kB inhibition by JSH-23 in E0771 cells abolished expression of inflammatory module, indicating that the mechanism of c-Myb suppression of the inflammatory signature involves negative regulation of NF-kB pathway.
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