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Genome wide analysis of BCL3 mediated chemotherapy resistance

ABSTRACT: We identify the atypical inhibitor-κB protein, Bcl3, as a novel biomarker in gliomas whose expression level predicts response to therapy. Bcl3 is found at 19q13 and its expression level in glioma is regulated by copy number alteration. Mechanistically, Bcl3 mediates mesenchymal differentiation and its presence promotes resistance to cytotoxic DNA damage.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80729 | GEO | 2018/07/21

REPOSITORIES: GEO

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Genome-wide analysis of macrophage gene expression upon Bcl3 knockdown

Project description:By binding to specific DNA elements, known collectively as “κB sites”, contained within the promoters/enhancers of target genes, NF-κB regulates gene expression. We found that the identity of the central base pair (bp) of κB sites profoundly impacts the transcriptional activity of NF-κB dimers. RelA dimers prefer an A/T bp at this position for optimum transcriptional activation (A/T-centric) and discriminate against G/C-centric κB sites. The p52 homodimer, in contrast, activates transcription from G/C-centric κB sites in complex with Bcl3 but represses transcription from the A/T-centric sites. The p52:Bcl3 complex binds to these two classes of κB sites in distinct modes permitting recruitment of coactivator, corepressor, or both coactivator and corepressor complexes in promoters containing G/C, A/T or both G/C and A/T-centric sites. Therefore, through sensing of bp differences within κB sites, NF-κB dimers modulate biological programs by activating, repressing and altering expression of effector genes. Total RNA extracted from bone marrow derived macrophages (BMDMs) with Bcl3 siRNA knockdown or mouse scramble siRNA knockdown were subjected to LPS stimulation.

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Project description:Peripherally induced regulatory T cells (pTregs) expressing the retinoic acid receptor-related orphan-receptor gamma t (RORγt) are indispensable for intestinal immune homeostasis. Previous studies have determined the role of the atypical NFκB inhibitor Bcl3 in the development of colitis. In this study we analyzed the influence of Bcl3 on pTreg development and functionality in healthy mice and under colitogenic conditions. Our findings reveal that expression of Bcl3, in health, limits not just the development of pTregs in a T cell intrinsic manner but also the formation of a RORγt+Helios+ double positive subset (DPTreg) expressing an activated transcriptional profile. Consequently, loss of Bcl3 in Tregs does not impede their suppressive capacity in a model of T cell transfer colitis but moreover leads to increased production of anti-inflammatory cytokines IL-10 and TGFβ. We further demonstrate that lack of Bcl3 in Tregs results in trans-differentiation towards Th17-like cells. Finally, we provide a Bcl3 dependent gene signature in pTregs including altered signaling of the cytokines IL-2, IL-6 and TNFα. We therefore conclude that expression of Bcl3 regulates the sensitivity of Tregs towards homeostatic cytokines and consequently limits the formation of an unphysiological number of RORγt+ Tregs.

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