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MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state

ABSTRACT: MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state

PROVIDER: PRJNA341715 | ENA |

REPOSITORIES: ENA

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MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [microarray]

Project description:We address the molecular mechanisms through which MYC promotes loss of cell identity and acquisition of stem cell-like traits, favouring the onset of tumorigenesis, by performing gene expression profile analyses in a transition from WT IMEC, IMEC over-expressing MYC and mammospeheres formed from IMEC-MYC (named M2). We then investigated the global gene expression profile of the fraction of cells hyper-activating the WNT pathway in M2 spheres, compared to the ones with low activation

2018-01-30 | GSE86407 | GEO

MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [ChIP-seq]

2018-01-30 | GSE86412 | GEO

MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state

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

2018-01-30 | GSE86416 | GEO

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.

Project description:Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermore, we demonstrate that the MYC-driven epigenetic reprogramming favors the formation and maintenance of tumor-initiating cells endowed with metastatic capacity. This study supports the notion that MYC-driven tumor initiation relies on cell reprogramming, which is mediated by the activation of MYC-dependent oncogenic enhancers, thus establishing a therapeutic rational for treating basal-like breast cancers.

| S-EPMC5844884 | biostudies-literature

Rank pathway activation attenuates mammary tumorigenesis by inducing senescence

Project description:Rank overexpression attenuates mammary tumorigenesis by inducing senescence in mammary epithelial cells but enhances tumor aggressiveness by increasing stemness.

2022-02-24 | GSE139675 | GEO

Rank pathway activation attenuates mammary tumorigenesis by inducing senescence

Project description:Rank pathway activation attenuates mammary tumorigenesis by inducing senescence

| PRJNA586861 | ENA

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors

Project description:This SuperSeries is composed of the following subset Series: GSE32727: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [human] GSE32904: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [mouse] Refer to individual Series

2012-07-23 | E-GEOD-32905 | biostudies-arrayexpress

Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context

Project description:This SuperSeries is composed of the following subset Series: GSE34857: Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context (ChIP-chip) GSE34858: Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context (mRNA) Refer to individual Series

2012-03-19 | E-GEOD-34859 | biostudies-arrayexpress

Homo sapiens

Project description:MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [microarray]

| PRJNA341702 | ENA

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [mouse]

Project description:The newly identified claudin-low subtype of cancer is believed to represent the most primitive breast malignancies, having arisen from transformation of an early epithelial precursor with inherent stemness properties and metaplastic features. Challenging this hypothesis, we show both in vitro and in vivo that transcription factors inducing epithelial-mesenchymal transition can drive the development of claudin-low tumors from differentiated mammary epithelial cells, by playing a dual role in cell transformation and dedifferentiation. Gene expression profiles of three independent Twist1 + Ras- transgenic mouse-derived metaplastic breast tumors (Breast Tumor A, B and C) and of two luminal MMTV-ERBB2/Neu-breast tumor-derived cell lines (1 and 2) were determined.

2012-07-23 | E-GEOD-32904 | biostudies-arrayexpress

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