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E-GEOD-34331

ABSTRACT: Transcription profiling by array of human breast cancer MCF-7 cells treated with novel compound F05 which promotes neurite growth on inhibitory substrates

OTHER RELATED OMICS DATASETS IN: PRJNA151493

PROVIDER: E-GEOD-34331 | ExpressionAtlas | 2014-07-03

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-34331-analysis-methods.tsv	Tabular
	E-GEOD-34331-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-34331-configuration.xml	Xml
	E-GEOD-34331-percentile-ranks.tsv	Tabular
	E-GEOD-34331.condensed-sdrf.tsv	Tabular

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Project description:Transcriptional profiling of human MCF-7 breast cancer cells comparing MCF-7 cells treated with control medium (DMEM/F12 + 0,5% BSA) with MCF-7 cells treated with conditioned medium of cancer-associated adipose tissue (CMCAAT) obtained from 2 breast cancer patients. Goal was to determine the effects of CMCAAT treatment on global MCF-7 gene expression. Two-condition experiment: MCF-7 control vs. CMCAAT treated cells. Biological replicates: 3 control replicates pooled as 1 (LL 1-2-4), 4 CMCAAT replicates (LL 6, LL 8, LL 9, LL 10)

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Project description:Heparins treated human breast cancer MCF-7 cell

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Transcription profiling by array of human hormone-responsive MCF-7 cells versus estrogen-deprived breast cancer cells

Project description:Estrogen deprivation using aromatase inhibitors is currently the standard of care for patients with estrogen-receptor (ER)-positive breast cancer. Unfortunately, prolonged estrogen deprivation leads to drug resistance (i.e. hormone-independent growth). We therefore used DNA microarray analysis to study the gene expression profiles of wild-type MCF-7 cells (which are sensitive to antihormone therapy) and long-term estrogen deprived MCF-7:5C and MCF-7:2A breast cancer cells (which are resistance to estrogen-deprivation; aromatase inhibitor resistant). Transcriptional profiling of wild-type MCF-7 cells and estrogen deprived MCF-7:5C and MCF-7:2A cells was performed using Affymetrix Human Genome U133 Plus 2.0 Array. Experiment Overall Design: We wanted to study the gene expression profiles of the different cell lines in their growth media without any drug treatment. Therefore, MCF-7, MCF-7:5C, and MCF-7:2A cells were grown in estrogen-free media (phenol red-free RPMI medium supplemented with 10% 4X dextran-coated charcoal-treated fetal bovine serum) until they were 70-80% confluent then RNA was extracted, labeled, and hybridized to the Affymetrix Human Genome U133 Plus 2.0 Arrays.

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Expression data of hormone-responsive MCF-7 cells versus estrogen-deprived MCF-7:5C and MCF-7:2A breast cancer cells

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MCF-7 Cell Derived Soluble Factors Define Growth of Vascular and Lymphatic Endothelial Cells: Modulatory Role of miR193a

Project description:Angiogenesis and Lymphangiogenesis plays a key role in promoting tumor growth and breast cancer progression as well as metastasis. Active angiogenic process within the tumor tissue is known to promote cancer/tumor growth via nutrient supply, moreover, soluble molecules secreted by lymphatic endothelial cells (ECs) promotes tumor growth. Hence is feasible that paracrine factors generated by breast cancer cells play a role in regulating tumor neovascularization by lymphatic and vascular ECs. Here using cultured VECs and LECs assessed the paracrine impact of MCF-7 breast cancer derived soluble factors on LEC and VEC growth (cell number), gene expression (micro array) and angiogenic proteins (protein array). Moreover, we explored the modulatory actions of miR193 on LEC and VEC growth driven by MCF-7 derived conditioned medium (MCF7-CM). We demonstrate that MCF7-CM differentially modulates VEC and LEC growth, i.e. induces VEC growth and inhibits LEC growth. Moreover, the growth actions of MCF7-CM were accompanied with differential modulation VEC and LEC growth regulatory genes, that were further altered by miR193 a pretreatment of MCF7 cells. Our findings provide in-depth analysis of MCF7-CM altered genes relevant for angiogenesis and lymphogenesis. The fact that vascular capillaries support growth and lymphatic capillaries play a role counteracting cancer growth (kill cancer cells), together with our observation in VECs and LECs, suggests that MCF-7 breast cancer cells differentially modulate vascular and lymphatic growth to facilitate their survival and growth. Since miR193a abrogates the effects of MCF7-CM, it may be an effective therapeutic tool against breast cancer.

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