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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas

ABSTRACT: The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas. They promote cancer cell dissemination by inducing an epithelial-to-mesenchymal transition (EMT) and by protecting cells from anoikis. We now have demonstrated that the sequentially related SNAI3 gene is aberrantly reactivated in human breast carcinomas. To compare the functional properties of the three SNAIL family members, the transcription factors were ectopically expressed in immortalized mammary epithelial cells. Immortalized human mammary epithelial cells (HMEC-hTERT cells) or MCF10A cells were infected with SNAIL retroviral expression constructs. The gene expression profiles of the resulting cell lines, cultured in standard conditions or after plating them 24h in low-adherent (LA) conditions, were performed.

ORGANISM(S): Homo sapiens

SUBMITTER: stÃ©phane ansieau

PROVIDER: E-GEOD-40690 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas

Project description:The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas. They promote cancer cell dissemination by inducing an epithelial-to-mesenchymal transition (EMT) and by protecting cells from anoikis. We now have demonstrated that the sequentially related SNAI3 gene is aberrantly reactivated in human breast carcinomas. To compare the functional properties of the three SNAIL family members, the transcription factors were ectopically expressed in immortalized mammary epithelial cells.

2013-09-30 | GSE40690 | GEO

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

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

A RNA-seq-based gene expression profiling of radiation-induced tumorigenic mammary epithelial cells

Project description:To understand tumorigenesis and cancer progression of mammary epithelium, we established a cell model combining over-expression of human telomerase reverse transcriptase gene (hTERT) and heavy-ion radiation from normal human mammary epithelial cells. We subsequently used RNA-seq method to acquire their transcriptomes from two characteristic cell lines, an immortal epithelial cell line (I_hMEC) and a tumorigenic epithelial cell line (T_hMEC), and to look for differentially expressed genes (DEGs) between immortalization and tumorigenicity. We identified 7,053 DEGs, of which 84 were not only highly expressed but also significantly regulated. We found that house-keeping (HK) genes and tissue-specific (TS) genes were regulated differently during tumorigenesis; HK genes tend to be activated but TS genes tend to be repressed. We looked into three important pathways in cancer development: p53 signaling, cell cycle, and apoptosis. Although both immortal and tumorigenic cells have infinite potential to replicate and can escape apoptosis, a great number of genes exhibited different modulation pattern between the two processes. We also found that a significant number of DEGs were involved in epigenetic modification of chromatins. In conclusion, these findings may provide novel biomarkers in studying tumorigenicity and further our understanding of cellular mechanism(s) in the transition from immortal to tumorigenic processes. 2 samples examined: immortalized human mammary epithelial cell (I_hMEC) and tumorigenic human mammary epithelial cell (T_hMEC)

2013-12-09 | E-GEOD-31310 | biostudies-arrayexpress

Gene expression profile of normal human mammary epithelial stem/progenitor and myoepithelial cells

Project description:There is increasing evidence that breast and other cancers originate from and are maintained by a small fraction of stem/progenitor cells with self-renewal properties. Whether such cancer stem/progenitor cells originate from normal stem cells based on initiation of a de novo stem cell program, by reprogramming of a more differentiated cell type by oncogenic insults or both remains unresolved. A major hurdle in addressing these issues is lack of immortal human stem/progenitor cells that can be deliberately manipulated in vitro. We present evidence that normal and human telomerase reverse transcriptase (hTERT)-immortalized human mammary epithelial cells (hMECs) isolated and maintained in DFCI-1 medium retain a fraction with progenitor cell properties. These cells co-express basal, luminal and stem/progenitor cell markers. Clonal derivatives of progenitors co-expressing these markers fall into two distinct types: K5+/K19- (Type I) and K5+/K19+ (Type II). We show that both types of progenitor cells have self-renewal and differentiation ability. Through microarray analysis, we want to identify genes and pathways linked to human mammary epithelial stem/progenitor cell self-renewal and differentiation. Normal human mammary epithelial cells (hMECs) were isolated from Reduction Mammoplasty and immortalized by hTERT. Type I K5+/K19- and Type II K5+/K19+ cell colonies were isolated from hTERT-immortalized hMECs and cultured in MEGM medium for self-renewal and differentiation. Total RNA isolated from Type I, Type II, and differentiated Myoepithelial (Myo) cells were used on Affymetrix microarrays.

2010-07-29 | E-GEOD-22580 | biostudies-arrayexpress

Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1 (ChIP-chip)

Project description:Epithelial-Mesenchymal Transition (EMT) is thought to contribute to cancer metastasis, but its underlying mechanisms are not well understood. To define early steps in this cellular transformation, we analyzed human mammary epithelial cells with tightly regulated expression of Snail-1, a master regulator of EMT. Following Snail-1 induction, epithelial markers were repressed within 6 hours and mesenchymal genes induced at 24 hours. Snail-1 binding to its target promoters was transient (6-48 hours) despite continued protein expression and it was followed by both transient and long-lasting chromatin changes. To generate a potent reversible EMT-inducing stimulus, we created a Snail-1 retroviral expression construct, using a fused estrogen receptor (ER) response element to mediate regulation by exogenous 4-hydroxy-tamoxifen (4-OHT). Since Snail-1 protein stability and nuclear localization are suppressed by GSK3-beta-mediated phosphorylation, we substituted the six targeted amino acids (ER-Snail-1(6SA)), thus conferring constitutive activity to the induced protein (Zhou et al., 2004, Pubmed ID 15448698). Infection of non-transformed, immortalized human mammary epithelial MCF10A cells with ER-Snail-1(6SA), followed by treatment with 4-OHT, triggered morphological and biomarker characteristics of EMT. At 0, 6, 48 and 120 hours after beginning exposure to 4-OHT in ethanol (or, for controls, ethanol only) we ChIPed Snail-1 and 6 histone marks. We perfomed two replicates of each, except we only had one replicate of H3K27Me3 at 6 hours.

2013-12-18 | E-GEOD-52591 | biostudies-arrayexpress

Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1 (gene expression)

Project description:Epithelial-Mesenchymal Transition (EMT) is thought to contribute to cancer metastasis, but its underlying mechanisms are not well understood. To define early steps in this cellular transformation, we analyzed human mammary epithelial cells with tightly regulated expression of Snail-1, a master regulator of EMT. Following Snail-1 induction, epithelial markers were repressed within 6 hours and mesenchymal genes induced at 24 hours. Snail-1 binding to its target promoters was transient (6-48 hours) despite continued protein expression and it was followed by both transient and long-lasting chromatin changes. To generate a potent reversible EMT-inducing stimulus, we created a Snail-1 retroviral expression construct, using a fused estrogen receptor (ER) response element to mediate regulation by exogenous 4-hydroxy-tamoxifen (4-OHT). Since Snail-1 protein stability and nuclear localization are suppressed by GSK3-beta-mediated phosphorylation, we substituted the six targeted amino acids (ER-Snail-1(6SA)), thus conferring constitutive activity to the induced protein (Zhou et al., 2004, Pubmed ID 15448698). Infection of non-transformed, immortalized human mammary epithelial MCF10A cells with ER-Snail-1(6SA), followed by treatment with 4-OHT, triggered morphological and biomarker characteristics of EMT. At 3, 6, 12, 24, 72 and 120 hours after beginning exposure to 4-OHT in ethanol (or, for controls, ethanol only) we extracted RNA and did gene expression analysis using microarrays. We perfomed three replicates of each.

2013-12-18 | E-GEOD-52592 | biostudies-arrayexpress

Antagonistic regulation of EMT by TIF1γ and Smad4 in mammary epithelial cells

Project description:TGFβ is known to be a potent inducer of EMT, a process involved in tumor invasion. TIF1γ has been reported to participate to TGFβ signaling. In order to understand the role of TIF1γ in TGFβ signaling and its requirement for EMT, we analyzed the TGFβ1 response of human mammary epithelial cell lines. A strong EMT increase was observed in TIF1γ-silenced cells after TGFβ1 treatment, whereas Smad4 inactivation completely blocked this process. In support of these observations, microarray data show that the functions of several TIF1γ target genes can be linked to EMT. As a negative regulator of Smad4, TIF1γ could be critical for the regulation of TGFβ signaling. This work highlights the molecular relationship between TIF1γ and Smad4 in TGFβ1 signaling and EMT. Total mRNA extractions were performed for 11 samples from transfected HMEC-TR. Replicates are rimo1, 6; rimo3, 9; rimo2, 7; rimo 4, 10 and rimo 5, 11. Rimo 8 is a single experiment. All RNA extractions were obtained from two independent cell cultures excepted for rimo8. Rimo 1, 6 are replicate for ctrl-; Rimo 3, 9 are replicate for ctrl+; Rimo 2, 7 are replicate for SiTIF-; Rimo 4, 10 are replicate for SiTIF+; Rimo8 is SiSmad4-; and Rimo5, 11 are replicate for SiSmad4+. ctrl means that HMEC-TR were transfected with an SiRNA scramble. "siSmad4" means that HMEC-TR were transfected with an SiRNA anti Smad4. "siTIF" means that HMEC-TR were transfected with an SiRNA anti TIF1γ. "-" means that cells were grown without TGFβ. "+" means that cells were treated with 5 ng/ml TGFβ1 for 24h.

2011-05-26 | E-GEOD-28448 | biostudies-arrayexpress

Transcriptome study of human mammary epithelial cells following exposure to polymeric Eudragit RS nanoparticles part 1

Project description:To further study the transcriptome of human mammary epithelial cells (HMEC 184) after exposure to polymeric Eudragit RS nanoparticles (ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to ENP. Changes in gene expression in HMEC 184 cells (50M-BM- % confluence) incubated with 25M-BM- M-BM-5g/mL ENPs (70M-BM- nm) for 24M-BM- h, and without incubation (control) were measured. Three biological replicates were performed as controls (US_01; US_02; US_04) and ENP exposed ones (US_6; US_07; US_08).

2013-08-01 | E-GEOD-45598 | biostudies-arrayexpress

Transcriptome study of human mammary epithelial cells following exposure to polymeric Eudragit RS nanoparticles part 2

Project description:To further study the transcriptome of human mammary epithelial cells (HMEC 184) after exposure to polymeric Eudragit RS nanoparticles (ENP), we investigate whole genome microarray expression to identify genes regulated by exposure or not to ENP. Changes in gene expression in HMEC 184 cells (90M-BM- % confluence) incubated with 25M-BM- M-BM-5g/mL ENPs (70M-BM- nm) for 24M-BM- h, and without incubation (control) were measured. Three biological replicates were performed as controls (US_09; US_10; US_11) and ENP exposed ones (US_12; US_13; US_14).

2013-08-01 | E-GEOD-45868 | biostudies-arrayexpress

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