Expression data from MCF7 cells: control or tuberin-depleted
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE68324 | GEO | 2015/04/28
SECONDARY ACCESSION(S): PRJNA282448
REPOSITORIES: GEO
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Project description:Analysis of the expression profiles of MCF7 cells transduced with a control shRNA and an TSC2-targeted shRNA (leading to tuberin depletion). MCF7 cells were cultured in standard conditions, transduced, selected with puromycin (pLKO.1 shRNA vectors) and processed for expression profiling.
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Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF. Four samples were harvested after lentiviral infection with either non-specific shRNA control or PDEF-targetting shRNA. All samples were subjected to hormone depletion for 48 hours. Each condition was performed in duplicate
2014-03-29 | E-GEOD-40985 | biostudies-arrayexpress
Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF.
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Project description:Elevated mitochondrial biogenesis and metabolism represent key features of breast cancer stem cells (CSCs), whose propagation is conducive to disease onset and progression. Therefore, interfering with mitochondria biology and function may be regarded as a useful approach to eradicate CSCs. Here, we used the breast cancer cell line MCF7 as a model system to interrogate how mitochondrial fission contributes to the development of mitochondrial dysfunction toward the inhibition of metabolic flux and stemness. We generated an isogenic MCF-7 cell line transduced with Mitochondrial Fission Factor (MCF7-MFF), which is primarily involved in mitochondrial fission. We evaluated the biochemical, molecular and functional properties of MCF7-MFF cells, as compared to control MCF7 cells transduced with the empty vector (MCF7-Control). We observed that MFF over-expression reduces both mitochondrial mass and activity, as evaluated using the mitochondrial probes MitroTracker Red and MitoTracker Orange, respectively. The analysis of metabolic flux using the Seahorse XFe96 revealed the inhibition of OXPHOS and glycolysis in MCF7-MFF cells, suggesting that increased mitochondrial fission may impair the biochemical properties of these organelles. Notably, CSCs activity, assessed by 3D-tumorsphere assays, was reduced in MCF7-MFF cells. A similar trend was observed for the activity of ALDH, a well-established marker of stemness. We conclude that enhanced mitochondrial fission may compromise CSCs propagation, through the impairment of mitochondrial function, possibly leading to a quiescent cell phenotype. Unbiased proteomic analysis revealed that proteins involved in mitochondrial dysfunction, oxidative stress-response, fatty acid metabolism and hypoxia signaling are among the most highly up-regulated in MCF7-MFF cells. Of note, integrated analysis of top regulatory networks obtained from unbiased proteomics in MCF7-MFF cells predicts that this cell phenotype activates signaling systems and effectors involved in the inhibition of cell survival and adhesion, together with the activation of specific breast cancer cell death programs. Overall, our study shows that unbalanced and abnormal activation of mitochondrial fission may drive the impairment of mitochondrial metabolic function, leading to inhibition of CSC propagation, and the activation of quiescence programs. Exploiting the potential of mitochondria to control pivotal events in tumor biology may, therefore, represent a useful tool to prevent disease progression.
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Project description:To interrogate the hypoxia response pathways affected by the depletion of CAIX in BC cells, we performed gene expression profiling using SurePrint G3 Human Gene Expression 60K microarrays in MDA-MB-231-shCAIX, MCF7-shCAIX and the respective control cells grown as multicellular spheroids under hypoxic or normoxic conditions. The human breast cancer cell lines MDA-MB-231 and MCF7 were purchased from the European Collection of Cell Cultures (ECACC, UK) and maintained as recommended by the manufacturer. To generate stable CAIX silenced cells, cell lines were transfected with a pool of three plasmids each encoding CAIX-specific shRNA (1 µg) and a negative control (NC) plasmids encoding scrambled shRNAs (1 µg) (Santa Cruz Biotechnology, TX, USA) using shRNA transfection medium and shRNA transfection reagent (Santa Cruz Biotechnology, USA) according to the manufacturers’ protocol. For selection of stably transfected cells, puromycin dihydrochloride (Santa Cruz Biotechnology, USA) was added to medium 48 h post-transfection (6 µg/ml for MCF7, 2 µg/ml for MDA-MB-231 cells). The transfected cells were plated at density 2e+3 cells per ml of serum-free DMEM/F12 medium supplemented with EGF (20ng/ml, R&D Systems, #236-EG-200), bFGF (10ng/ml, SantaCruz, #sc-4573), hydrocortisone (50 ng/ml, Sigma-Aldrich, #H0135-1MG) and 1B27 (Invitrogen, #17504001) and grown as multicellular spheroids for 5 days. To establish hypoxic conditions, the cells were cultured at 1% oxygen, 94% N2 and 5% CO2 at 37oC using humidified multi-gas incubator (Sanyo, Sanyo Electric Co.,Ltd.) for 48 hours. The normoxic control cells were incubated at 37oC with 5% CO2 in a humidified incubator (Panasonic, Panasonic Healthcare Co., Ltd.). The efficiency of CAIX silencing was assessed by qRT-PCR and immunofluorescence before the experiments.
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