Effect of overexpression of EPIC1 on gene expression in MCF7 cells [RNA-seq I]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE229721 | GEO | 2025/06/10
REPOSITORIES: GEO
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Project description:Effect of overexpression of EPIC1 on gene expression in MCF7 cells [RNA-seq I]
| PRJNA955706 | ENA
Project description:In an integrated analysis of long noncoding RNA (lncRNA) epigenetic alterations in 6475 tumor samples and 781 cancer cell lines, we characterized the epigenetic landscape for 1,006 epigenetically activated and 1,117 epigenetically silenced lncRNAs across 20 cancer types. Combining bioinformatics analyses and functional validation, we identified epigenetically induced lncRNA 1 (EPIC1) as a potential oncogene. EPIC1 is epigenetically activated in 15 cancer types and correlated with poor survival of breast cancer. In EPIC1 hypermethylated cancer cell lines, its expression can be induced by demethylating agent in a time- and dose-dependent manner. Knockdown of EPIC1 inhibits MYC targets expression, leads to cell cycle arrest, inhibits colony formation, and decreases cancer cell growth in vitro and in vivo. Mechanistically, EPIC1 directly interacts with MYC 148-220 aa region through its 5’ end. Overexpression of EPIC1 increases MYC targets expression and promotes cell proliferation, which can be abolished by the MYC knockdown.
2018-05-03 | GSE98538 | GEO
Project description:Chromatin immunoprecipitation assays followed by sequencing (ChIP-Seq) of H3K27me3 in MCF-7 cells overexpressing EPIC1.
2025-06-10 | GSE229720 | GEO
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:To further identify the downstream target of CD44-dependent lamellipodia formation during luminal type BrCa progression, we firstly established a stable cell line by transfection of CD44 cDNA into MCF7 cells which expresses low level of CD44. Then we used RNA-sequencing (RNA-seq) to compare mRNA expression profiles between the MCF7vector and MCF7CD44 cells.
2023-09-20 | GSE233209 | GEO
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. 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:To investigate and determine the function of EPIC1 in cancer cells, we knockdown EPIC1 in Hs578T, A2780, and A2780cis cells using siRNA.
2025-06-10 | GSE229722 | 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:ChIP-Seq of H3K27me3 in MCF-7 cells overexpressing EPIC1
| PRJNA955704 | ENA