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Expression of SV40 TAg signature in MDAMB231 cells, tumors, and normal human mammary epithelial cells (M98040 and M99005)

ABSTRACT: MDAMB231 cells express the SV40TAg signature. The normal mammary epithelial tissue does not express the signature. CK0082, Empty1 and Gata3 samples are not reported in this manuscript

ORGANISM(S): Homo sapiens

PROVIDER: GSE25487 | GEO | 2011/09/01

SECONDARY ACCESSION(S): PRJNA134703

REPOSITORIES: GEO

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Expression of SV40 TAg signature in MDAMB231 cells, tumors, and normal human mammary epithelial cells (M98040 and M99005)

Project description:MDAMB231 cells express the SV40TAg signature. The normal mammary epithelial tissue does not express the signature. CK0082, Empty1 and Gata3 samples are not reported in this manuscript We used microarrays to determine whether the MDAMB231 cell lines and tumors express the SV40Tag signature (91 gene signature).

2011-08-31 | E-GEOD-25487 | biostudies-arrayexpress

Expression of SV40 TAg signature in MDAMB231 cells, tumors, and normal human mammary epithelial cells (M98040 and M99005)

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The gene expression response of MCF7 and MDAMB231 to glutamine deprivation

Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies. Gene expression analysis in MCF7 and MDAMB231 cultured with or without glutamine for 24h

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Effect of Omomyc treatment on human TNBC MDAMB231 cell line

Project description:Analysis of MDAMB231 cells treated with 12.8 µM Omomyc or vehicle (PBS) for three days.

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LARP iCLIP in MDAMB231 cell lines

Project description:LARP iCLIP in MDAMB231 cell lines

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MDAMB231 transcriptome response to SKP2 knockdown

Project description:MDAMB231 transcriptome response to SKP2 knockdown

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Aberrant Proliferation of Differentiating Alveolar Cells Induces Hyperplasia in Resting Mammary Glands of SV40-TAg Transgenic Mice.

Project description:WAP-T1 transgenic mice express SV40-TAg under control of the whey acidic protein (WAP) promoter, which directs activity of this strong viral oncogene to luminal cells of the mammary gland. Resting uniparous WAP-T1 glands develop hyperplasia composed of TAg positive cells prior to appearance of advanced tumor stages. We show that cells in hyperplasia display markers of alveolar differentiation, suggesting that TAg targets differentiating cells of the alveolar compartment. The glands show significant expression of Elf5 and milk genes (Lalba, Csn2, and Wap). TAg expressing cells largely co-stain with antibodies to Elf5, lack the epithelial marker Sca1, and are hormone receptor negative. High expression levels of Elf5 but not of milk genes are also seen in resting glands of normal BALB/c mice. This indicates that expression of Elf5 in resting WAP-T1 glands is not specifically induced by TAg. CK6a positive luminal cells lack TAg. These cells co-express the markers prominin-1, CK6a, and Sca1, and are positive for hormone receptors. These hormone sensitive cells localize to ducts and seem not to be targeted by TAg. Despite reaching an advanced stage in alveolar differentiation, the cells in hyperplasia do not exit the cell cycle. Thus, expression of TAg in conjunction with regular morphogenetic processes of alveologenesis seem to provide the basis for a hormone independent, unscheduled proliferation of differentiating cells in resting glands of WAP-T1 transgenic mice, leading to the formation of hyperplastic lesions.

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The gene expression response of MCF7 and MDAMB231 to glutamine deprivation

2012-01-01 | GSE26370 | GEO

Effect of Omomyc treatment on human TNBC MDAMB231 cell line

Project description:Effect of Omomyc treatment on human TNBC MDAMB231 cell line

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Bigh3 silencing increases retinoblastoma tumor growth in the murine SV40-TAg-Rb model.

Project description:BIGH3, a secreted protein of the extracellular matrix interacts with collagen and integrins on the cell surface. BIGH3 can have opposing functions in cancer, acting either as tumor suppressor or promoter by enhancing tumor progression and angiogenesis. In the eye, BIGH3 is expressed in the cornea and the retinal pigment epithelium and could impact on the development of retinoblastoma, the most common paediatric intraocular neoplasm. Retinoblastoma initiation requires the inactivation of both alleles of the RB1 tumor suppressor gene in the developing retina and tumor progression involves additional genomic changes. To determine whether BIGH3 affects retinoblastoma development, we generated a retinoblastoma mouse model with disruption of the Bigh3 genomic locus. Bigh3 silencing in these mice resulted in enhanced tumor development in the retina. A decrease in apoptosis is involved in the initial events of tumorigenesis, followed by an increased activity of the pro-survival ERK pathway as well as an upregulation of cyclin-dependent kinases (CDKs). Taken together, these data suggest that BIGH3 acts as a tumor suppressor in the retina.

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