Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Differential Gene Expression between MCF10A and MCF7 cells

ABSTRACT: These RNA-seq data were generated to correlate with genomic interaction data in a related Hi-C analysis. MCF10A is a normal-like mammary epithelial cell line and MCF7 is a transformed estrogen responsive breast cancer cell line derived from a metastatic site; both are commonly used in models of breast cancer progression. Analysis revealed a set of genes related to repression of WNT signalling that were both up-regulated in MCF7 and located in genomic regions that had transitioned from closed to open structure in MCF7. RNA-seq of MCF10A and MCF7 cells. 3 replicates each. Sequencing was strand-specific and conducted on ribo-depleted RNA.

ORGANISM(S): Homo sapiens

SUBMITTER: Jane Lian

PROVIDER: E-GEOD-71862 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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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Differential Gene Expression between MCF10A and MCF7 cells

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