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Reprogramming breast cancer cells to breast cancer stem cells-like by the POU1F1 transcription factor

ABSTRACT: Reprogramming breast cancer cells to breast cancer stem cells-like by the POU1F1 transcription factor

PROVIDER: PRJNA1214747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32092569_1.fastq.gz	Fastqsanger.gz
	SRR32092569_2.fastq.gz	Fastqsanger.gz
	SRR32092570_1.fastq.gz	Fastqsanger.gz
	SRR32092570_2.fastq.gz	Fastqsanger.gz
	SRR32092571_1.fastq.gz	Fastqsanger.gz

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Reprogramming breast cancer cells to breast cancer stem cells-like by the POU1F1 transcription factor

Project description:POU1F1 (also named PIT-1) is a well-known transcription factor involved in embryonic and adult pituitary development that has also been analyzed for its role in breast cancer . This study provides compelling evidence of POU1F1 in reprogramming breast cancer cells into BCSC-like. Our data demonstrates that POU1F1 induces a BCSC-like phenotype in breast tumor cells by deregulating markers such as CD24, CD44, CD133, and ALDH. These phenotypic modifications are correlated with functional changes, i.e. higher clonogenicity, increased mammospheres formation, and increased glycolysis metabolism. In addition, using in vivo immunodeficient mice models we found that a subpopulation of ALDHhigh cells from the POU1F1 overexpressing MCF-7 cells possess high tumor-initiating capacity, high resistance to chemo- and radiotherapy, and reduced overall survival. Mechanistically, POU1F1 induces an increase in IL-6 mRNA expression and raises IL-6 in the culture medium. This activates the IL-6/JAK/STAT3 pathway, which in turn increases ALDH mRNA expression.

2025-05-06 | GSE287812 | GEO

Study of epithelial-mesenchymal transition induced by POU1F1 in normal breast cells

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Project description:The transcription factor POU1F1 plays an important role in breast cancer. It has been described that POU1F1 is capable of regulating the expression of different genes involved in cell proliferation, apoptosis and cell plasticity. The mechanism by which POU1F1 carries out these regulations is still unknown, and epigenetics is one of the possible causes. Epigenetics refers to modifications in gene expression that are heritable through cell division and that occur without changes in the DNA sequence. DNA methylation is one of the most important epigenetic mechanisms.

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GATA3-mediated chromatin reprogramming in breast cancer cells

Project description:Pioneer transcription factors bind to silent chromatin, and initiate cell fate conversion. One potential pioneer factor, GATA3, is a critical component for multiple cellular programs. GATA3 is of particular interest as it regulates gene expression in breast cancers, and low expression correlates with poor prognosis. Here we demonstrate the pioneering activity of GATA3 utilizing a cellular reprogramming system (the mesenchymal-epithelial transition) in breast cancer cells. During the epithelial transition, GATA3 catalyzes chromatin reprogramming by inducing chromatin opening, active enhancer modifications, and nucleosome remodelling. We determined that the transactivation domain is required for this chromatin reprogramming. Importantly, a mutant lacking the transactivation domain possessed the chromatin binding ability but failed to create open chromatin, suggesting binding alone is not sufficient to induce open chromatin. These data illustrate a fundamental mechanism of GATA3-mediated gene regulation, and provide evidence for a pre-engagement state of closed chromatin bound by a pioneer factor.

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