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Tumor suppressor FRMD3 Controls Mammary Epithelial Cells Fate Decision via Notch signaling pathway

ABSTRACT: Tumor suppressor FRMD3 Controls Mammary Epithelial Cells Fate Decision via Notch signaling pathway

PROVIDER: PRJNA1057302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27352923.fastq.gz	Fastqsanger.gz
	SRR27352924.fastq.gz	Fastqsanger.gz
	SRR27352925.fastq.gz	Fastqsanger.gz
	SRR27352926.fastq.gz	Fastqsanger.gz
	SRR27352927.fastq.gz	Fastqsanger.gz

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Tumor suppressor FRMD3 Controls Mammary Epithelial Cells Fate Decision via Notch signaling pathway

Project description:Luminal to basal transition in mammary gland is accompanied by the changes of epithelial cell lineage plasticity, however, the underlying mechanism remains elusive. Here, we demonstrated that loss of the scaffold protein FRMD3 in breast cancer predicts poor outcomes. Knockout of Frmd3 inhibits mammary gland lineage development and induces mammary epithelium cells (MECs) stemness, and later on emerge of TNBC. Loss of Frmd3 in PyMT mice results in luminal to basal phenotype transition. Single- MEC mRNA sequencing analysis indicated that knockout of Frmd3 corresponds to inhibition of Notch signaling pathway. Mechanistically, FRMD3 assists Dishevelled-2 degradation via enhancing its interaction with the deubiquitinase USP9x. FRMD3 also interrupts the interaction of Dishevelled-2 with CK1, FOXK1, FOXK2 and NICD, causing a decrease in Dishevelled-2 phosphorylation, entry into the nucleus and impairing the Notch-dependent luminal epithelial lineage plasticity in MECs respectively. Taken together, FRMD3 is a tumor suppressor and an endogenous activator of the Notch signaling pathway that regulates mammary epithelial cell lineage plasticity.

2024-07-10 | GSE252083 | GEO

Telomere Shortening Impairs PGC Fate Decision

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High apoptotic threshold mediates p53 dependent decision between arrest and apoptosis

Project description:In response to stress, the p53 tumor suppressor induces arrest or apoptosis by transcriptionally regulating genes that mediate these processes. It has been proposed that the levels of p53 can influence the choice between these different outcomes, but the mechanisms involved are not clear. To gain mechanistic understanding of this p53-dependent cell fate decision, we generated a p53 inducible system that allowed tight regulation of p53 expression in human mammary epithelial cells. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Using microarray and chromatin immunoprecipitation analysis, we showed that low and high levels of p53 bind to and activate the same set of pro arrest and pro apoptotic target genes, induced to lower and higher levels, respectively. We propose that the cell fate decision between arrest and apoptosis in these cells is determined by a higher threshold required for p53 dependent apoptosis. We suggest that high level p53 activation is crucial in order to achieve maximum efficacy of p53 targeted cancer therapies.

2011-07-19 | E-GEOD-30753 | biostudies-arrayexpress

Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

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Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

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High apoptotic threshold mediates p53 dependent decision between arrest and apoptosis

2011-07-20 | GSE30753 | GEO

Tumor suppressor FRMD3 controls mammary epithelial cell fate determination via notch signaling pathway.

Project description:The luminal-to-basal transition in mammary epithelial cells (MECs) is accompanied by changes in epithelial cell lineage plasticity; however, the underlying mechanism remains elusive. Here, we report that deficiency of Frmd3 inhibits mammary gland lineage development and induces stemness of MECs, subsequently leading to the occurrence of triple-negative breast cancer. Loss of Frmd3 in PyMT mice results in a luminal-to-basal transition phenotype. Single-cell RNA sequencing of MECs indicated that knockout of Frmd3 inhibits the Notch signaling pathway. Mechanistically, FERM domain-containing protein 3 (FRMD3) promotes the degradation of Disheveled-2 by disrupting its interaction with deubiquitinase USP9x. FRMD3 also interrupts the interaction of Disheveled-2 with CK1, FOXK1/2, and NICD and decreases Disheveled-2 phosphorylation and nuclear localization, thereby impairing Notch-dependent luminal epithelial lineage plasticity in MECs. A low level of FRMD3 predicts poor outcomes for breast cancer patients. Together, we demonstrated that FRMD3 is a tumor suppressor that functions as an endogenous activator of the Notch signaling pathway, facilitating the basal-to-luminal transformation in MECs.

| S-EPMC11221522 | biostudies-literature

Bcl6 mediates CD8+ T cell fate decision in cancer

Project description:Bcl6 mediates CD8+ T cell fate decision in cancer

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [array]

Project description:Overexpression of the oncogene MEF2C oposses NOTCH signalling in T versus B lineage decision, driving leukemia in the thymus context

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Effects of acute Notch activation on the mammary epithelial compartment in vivo

Project description:Notch signaling is widely implicated in mouse mammary gland development and tumorigenesis. To investigate the effects of acute activation of Notch signaling in the mammary epithelial compartment, we generated bi-transgenic MMTV-rtTA; TetO-NICD1 (MTB/TICNX) mice that conditionally express a constitutively active NOTCH1 intracellular domain (NICD1) construct in the mammary epithelium upon doxycycline administration.

2015-05-12 | GSE51628 | GEO

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