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Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE195716 | GEO | 2022/10/19

REPOSITORIES: GEO

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Breast cancer plasticity is restricted by a LATS1-NCOR1 repressive axis.

Project description:Breast cancer, the most frequent cancer in women, is generally classified into several distinct histological and molecular subtypes. However, single-cell technologies have revealed remarkable cellular and functional heterogeneity across subtypes and even within individual breast tumors. Much of this heterogeneity is attributable to dynamic alterations in the epigenetic landscape of the cancer cells, which promote phenotypic plasticity. Such plasticity, including transition from luminal to basal-like cell identity, can promote disease aggressiveness. We now report that the tumor suppressor LATS1, whose expression is often downregulated in human breast cancer, helps maintain luminal breast cancer cell identity by reducing the chromatin accessibility of genes that are characteristic of a "basal-like" state, preventing their spurious activation. This is achieved via interaction of LATS1 with the NCOR1 nuclear corepressor and recruitment of HDAC1, driving histone H3K27 deacetylation near NCOR1-repressed "basal-like" genes. Consequently, decreased expression of LATS1 elevates the expression of such genes and facilitates slippage towards a more basal-like phenotypic identity. We propose that by enforcing rigorous silencing of repressed genes, the LATS1-NCOR1 axis maintains luminal cell identity and restricts breast cancer progression.

| S-EPMC9705295 | biostudies-literature

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [MARS-seq]

Project description:The tumor suppressor LATS1, whose expression is often downregulated in human breast cancer, helps maintain luminal breast cancer cell identity by keeping basal-specific genes in a closed chromatin state, preventing their spurious activation. This is achieved via interaction of LATS1 with the NCOR1 nuclear corepressor and recruitment of HDAC1,driving histone H3K27 deacetylation near NCOR1-repressed “basal” genes. Consequently, decreased expression of LATS1 elevates the expression of such “basal” genes and promotes luminal-to-basal slippage.

2022-10-19 | GSE195715 | GEO

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [ATAC-seq]

2022-10-19 | GSE195714 | GEO

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis

Project description:Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis

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Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [MARS-seq]

Project description:Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [MARS-seq]

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Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [ATAC-seq]

Project description:Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [ATAC-seq]

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The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate.

Project description:Placental development relies on coordinated cell fate decisions governed by signalling inputs. However, little is known about how signalling cues are transformed into repressive mechanisms triggering lineage-specific transcriptional signatures. Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with the Nuclear Receptor Co-Repressor Complex 1 and 2 (NCoR1/2) and recruits it to key trophoblast genes. Genetic ablation of Erf or Tbl1x (a component of the NCoR1/2 complex) abrogates the Erf/NCoR1/2 interaction. This leads to mis-expression of Erf/NCoR1/2 target genes, resulting in a TSC differentiation defect. Mechanistically, Erf regulates expression of these genes by recruiting the NCoR1/2 complex and decommissioning their H3K27ac-dependent enhancers. Our findings uncover how the Fgf/Erf/NCoR1/2 repressive axis governs cell fate and placental development, providing a paradigm for Fgf-mediated transcriptional control.

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LATS1 and LATS2 suppress breast cancer progression by maintaining cell identity and metabolic state

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-28 | GSE116818 | GEO

LATS2 regulates repressive epigenetic integrity via regulation of Polycomb repressive complex 2

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-25 | E-GEOD-63538 | biostudies-arrayexpress

Gene expression profiles in mouse livers depleted of HDAC3 or NCOR1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-11-25 | E-GEOD-49388 | biostudies-arrayexpress