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Biology subjects

Henneman, L.

Publications and source records attributed to Henneman, L..

2 recordsLinked to original sources

GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers

WNT4 is critical for epithelial side branching in the mammary gland. In both mice and humans, its expression is tightly regulated and restricted to hormone-responsive, mature luminal cells. Although generally assumed to act downstream of progesterone, the molecular mechanisms that control lineage-specific induction of WNT4 gene expression remain unknown. Here we functionally dissect the cis-acting enhancer network and spatiotemporal transcriptional mechanisms that regulate WNT4 expression in the mouse mammary gland and the human breast. We identify Grainyhead-like (GRHL) proteins as luminal-specific pioneer factors that bind to a conserved distal chromatin hub. The progesterone receptor (PGR) binds to different cis-acting elements that contact the hub via 3D chromatin looping to induce WNT4 expression. More generally, this model explains how the interplay between endocrine signaling and dynamic molecular interactions at the physical chromatin level can be translated into robust gene expression patterns on the tissue scale. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=102 SRC="FIGDIR/small/648333v1_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@ddca48org.highwire.dtl.DTLVardef@10b3d69org.highwire.dtl.DTLVardef@ecea45org.highwire.dtl.DTLVardef@86d00_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

MYC promotes immune-suppression in TNBC via inhibition of IFN signaling

Immune checkpoint inhibitor (ICI) treatment has thus far shown limited efficacy in triple-negative breast cancer (TNBC) patients, presumably due to sparse or unresponsive tumor-infiltrating lymphocytes. We reveal a strong correlation between MYC expression and loss of immune signatures in human TNBC. In mouse models of BRCA1-proficient and -deficient TNBC, MYC overexpression dramatically decreased lymphocyte infiltration in tumors, along with immune signature loss. Likewise, MYC overexpression suppressed inflammatory signaling induced by BRCA1/2 inactivation in human TNBC cell lines. Moreover, MYC overexpression prevented the recruitment and activation of lymphocytes in co-cultures with human and mouse TNBC models. Chromatin immunoprecipitation (ChIP)-sequencing revealed that MYC directly binds promoters of multiple interferon-signaling genes, which were downregulated upon MYC expression. Finally, MYC overexpression suppressed induction of interferon signaling and tumor growth inhibition by a Stimulator of Interferon Genes (STING) agonist. Together, our data reveal that MYC suppresses innate immunity and facilitates immune escape, explaining the poor immunogenicity of MYC-overexpressing TNBCs. Statement of SignificanceMYC suppresses recruitment and activation of immune cells in TNBC by repressing the transcription of interferon genes. These findings provide a mechanistic rationale for the association of high MYC expression levels with immune exclusion in human TNBCs, which might underlie the relatively poor response of many TNBCs to ICI.

cancer biology↗