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

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE32905 | GEO | 2012/07/24

SECONDARY ACCESSION(S): PRJNA146583

REPOSITORIES: GEO

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Similar Datasets

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

Project description: Not available

| S-ECPF-GEOD-32905 | biostudies-other

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

Project description: Not available

| S-EPMC3359981 | biostudies-literature

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

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

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. Human mammary epithelial cells (HMEC) were sequentially immortalized by hTert (HMEC-hTert), transduced with Twist1 or Zeb2 or Zeb1 and then with H-RasG12V. The gene expression profiles of the resulting HMEC-hTert-Twist1+Ras, HMEC-hTert-Zeb1+Ras and HMEC-hTert-Zeb2+Ras cell lines were defined. HMEC-hTert-Twist1+Ras and HMEC-hTert-Zeb2+Ras cell lines were additionally cultured in presence of TGFM-CM-^C? and their gene expression profiles were determined. The parental HMEC-hTert, the luminal MCF7 and the basal B MDMB157cell lines were used as controls.

2012-07-23 | E-GEOD-32727 | biostudies-arrayexpress

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

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

2012-07-24 | GSE32727 | GEO

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

2012-07-24 | GSE32904 | GEO

An EMT–primary cilium–GLIS2 signaling axis regulates mammogenesis and claudin-low breast tumorigenesis

Project description: Not available

| S-EPMC8550236 | biostudies-literature

EMT tumorigenesis in the mouse mammary gland.

Project description: Not available

| S-EPMC2754828 | biostudies-literature

An EMT-primary cilium-GLIS2 signaling axis regulates mammogenesis and claudin-low breast tumorigenesis

Project description:The Epithelial–Mesenchymal Transition (EMT) and primary ciliogenesis induce stem cell properties in basal Mammary Stem Cells (MaSCs) to promote mammogenesis, but the underlying mechanisms remain incompletely understood. Here, we show that EMT transcription factors promote ciliogenesis upon intermediate EMT transition states by activating ciliogenesis inducers, including FGFR1. The resulting primary cilia promote BBS11-dependent ubiquitination and inactivation of a central signaling node, GLIS2. We show that GLIS2 inactivation promotes MaSC stemness, and GLIS2 is required for normal mammary gland development. Moreover, GLIS2 inactivation is required to induce the proliferative and tumorigenic capacities of the Mammary-Tumor-initiating cells (MaTICs) of claudin-low breast cancers. Claudin-low breast tumors can be segregated from other breast tumor subtypes based on a GLIS2-dependent gene expression signature. Collectively, our findings establish molecular mechanisms by which EMT programs induce ciliogenesis to control MaSC and MaTIC biology, mammary gland development, and claudin-low breast cancer formation.

2021-10-05 | GSE173788 | GEO

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