Project description:Genome-wide expression analysis of MCF-10A and MCF-7 where miR-204 and miR-211 are overexpressed. The characteristics of differentially expressed genes in both cell lines derives the cells toward being oncogenic.
Project description: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.
Project description: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.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC).
Project description:We explored intron retention patterns in normal breast epithelial cells (MCF10A) and estrogen receptor positive (ER+) breast cancer cells (MCF7).
Project description:Small membrane-derived extracellular vesicles have been proposed to participate in several cancer diseases, including breast cancer. We performed phosphoproteomic analysis of breast cancer-derived small extracellular vesicles (sEVs) to provide insight into the molecular and cellular regulatory mechanisms important for breast cancer tumor progression and metastasis. We examined 3 cell lines as models for breast cancer: MCF10A (non-metastatic), MCF7 (estrogen and progesterone receptor positive, metastatic) and MDA-MB-231 (triple-negative, highly metastatic). To obtain a comprehensive overview of the sEV phosphoproteme derived from each cell line, an effective enrichment phosphopeptide techniques with IMAC and TiO2, followed by LC-MS/MS was achieved. In total, 2003 phosphopeptides on which 207, 854 and 1335 have been identified in MCF10A, MCF7 and MDA-MB-231cell lines, respectively. These phosphorylation sites were mapped to 855 distinct proteins, covering a wide range of functions. These proteins are associated with larger number of diseases and the most common diseases are related to cancer. Among the phosphoproteins identified, we validated four enzymes associated to cancer and present only in sEVs isolated from MCF7 and MDA-MB-231 cell lines: ATP citrate lyase (ACLY), phosphofructokinase-M (PFKM), Sirtuin-1 (SIRT1) and Sirtuin-6 (SIRT6). With the exception of PFKM, the specific activity of these enzymes was significantly higher in MDA-MB-231 when compared with MCF10A-derived sEVs. This study demonstrates that sEVs contain functional metabolic enzymes that could be further explored for their potential in early BC diagnostic and therapeutic applications.
Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101).
Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101). Two-condition experiment, MCF10A-vector control vs. MCF10A-TRIM29 shRNA cells; MCF7-vector control vs. MCF7-TRIM29 cells.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC). After establishing MCF7-luc anti-miR-27b, MCF7-luc miR-27b o.e. and MCF7-luc anti-NC using lentivirus vector, we performed the microarray analysis.
Project description:The expression levels of tRNA-derived small RNA, known as tsRNA, were interrogated in the following parental cell lines: MCF10A normal-like mammary epithelial cell, MCF7, MCF10AT1, MCF10CA1a, and MDA-MB-231 breast cancer cells. In addition, tsRNA expression was determined after shRNA-inhibition of RUNX1 in MCF10A cells or RUNX1 induction in MCF10CA1a cells.
