Genome-wide analysis of senecent MCF7 cells induced by irridiation and ectopic overexpression of p21
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PROVIDER: PRJNA429037 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of genes in senescent MCF7 cells induced by irridiation and ectopic expression of p21
2019-04-25 | GSE108895 | GEO
Project description:A mass spectrometry-based proteomics analysis was performed to study the protein binders of p21 in MCF7 cells during the progression and maintenance of cellular senescence.
2024-06-02 | PXD042908 | Pride
Project description:PTHrP overexpression in MCF7 cells
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Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression.
2011-06-01 | GSE26454 | GEO
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.
2020-10-16 | PXD020802 | Pride
Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.
2011-06-01 | E-GEOD-26454 | biostudies-arrayexpress
Project description:A PTHrP construct expressing full-length secreted PTHrP (-36-139aa) was stably expressed in MCF7 cells. The goal of the study was to determine the gene targets of PTHrP in human MCF7 breast cancer cells.
2018-05-30 | GSE110713 | GEO
Project description:As we clarified before, the FOXP3 gene is an X-linked tumor suppressor gene in mammary carcinoma in both human and mouse. We also clarified that the ERBB2 and SKP2 oncogenes were transcriptionally under control of the FOXP3 gene product in mammary epithelial cells. In order to further clarify the FOXP3 down stream target genes in human breast cancer cells, we planed to conduct a microarray analysis of FOXP3-induced gene expression profiling. MCF7, a human breast cancer cell line, with FOXP3-tet-off system was cultured with and without Doxycyclin for 2 days. In the MCF7 cell cultured without Dox, the FOXP3 transcript was significantly induced as compared to the MCF7 cultured with Dox. Total RNA from MCF7 with and wihtout Dox were extracted by Qiagen's RNeasy column and they were applied to Affymetrix Human U133 2.0 array according to the manufacture's protocol. We clarified as yet unknown FOXP3 target genes in human epithelial cells, e.g., the p21 gene, by this analysis.
2009-08-12 | E-MTAB-73 | biostudies-arrayexpress
Project description:Overexpression of p21 in NEMOM-NM-^Thepa animals protects against DNA damage, acceleration of hepatocarcinogenesis and cholestasis. As strengthened by our LPS stimulation experiments, we identified a novel protective role of p21 against DNA damage. Expression profiling of livers from wild type, NEMO, and NEMO-P21 null mice.
2015-03-01 | E-GEOD-61100 | biostudies-arrayexpress
Project description:effect of CD44 overexpression on luminal type breast cancer cell MCF7
| PRJNA975469 | ENA