Identification of EMT related genes in mcf10 cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE8430 | GEO | 2008/03/24
SECONDARY ACCESSION(S): PRJNA101491
REPOSITORIES: GEO
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Project description:In vitro studies on immortalized breast MCF10A cells were additionally performed to assess the phenotypic and genetic changes associated to mesenchymal transformation of breast cells and to their epithelial plasticity. To further study the molecular events associated to the cell plasticity of MCF10A cells, we decided to characterize the genetic programs modulated during the phenotypic changes by cDNA microarrays analysis. Cells were grown to 10-20% (sparse) or 80-100% confluence (confluent), and the corresponding RNAs were extracted and hybridized onto cDNA microarrays.
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Project description:Employing MCT-1 oncogene mediated transformation of immortalized breast epithelial MCF10A cells; we characterized the largely reciprocal association of these two RBPs with target mRNAs and their influence on protein expression vis-à-vis cellular transformation. Using a ribonomics approach, we identified mRNAs from cancer-related pathways whose association with AUF1 and/or HuR were altered when comparing immortalized with transformed MCF10A cells. Significantly, we were able to demonstrate that knockdown of HuR expression using RNA interference, reduced anchorage-independent growth capacity in transformed MCF10A cells as well as decreased protein expression of a number of validated target genes. Our data demonstrate that the global alterations in binding of HuR and AUF1 with target transcripts have a critical role in post-transcriptional regulation of genes encoding proteins involved in breast epithelial cell transformation.
2008-07-29 | GSE12215 | GEO
Project description:Employing MCT-1 oncogene mediated transformation of immortalized breast epithelial MCF10A cells; we characterized the largely reciprocal association of these two RBPs with target mRNAs and their influence on protein expression vis-à-vis cellular transformation. Using a ribonomics approach, we identified mRNAs from cancer-related pathways whose association with AUF1 and/or HuR were altered when comparing immortalized with transformed MCF10A cells. Significantly, we were able to demonstrate that knockdown of HuR expression using RNA interference, reduced anchorage-independent growth capacity in transformed MCF10A cells as well as decreased protein expression of a number of validated target genes. Our data demonstrate that the global alterations in binding of HuR and AUF1 with target transcripts have a critical role in post-transcriptional regulation of genes encoding proteins involved in breast epithelial cell transformation. In this study, using a microarray approach we demonstrate that the dynamic global changes in association of two RBPs, HuR and AUF1, with cancer-related mRNAs have important influence on cell transformation in a MCT-1-mediated breast epithelial transformation model.
2008-07-29 | E-GEOD-12215 | biostudies-arrayexpress
Project description:PHF8 exerts distinct functions in different types of cancer. However, the mechanisms underlying its specific functions in each case remain obscure. To establish whether overexpression of PHF8 regulates the TGF-β induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-β1 for 0, 24, 48 and 72 hours and performed RNA-seq in biological duplicates. Our data indicated that EMT gene signatures were significantly enriched in MCF10A-PHF8 cells with TGF-β1 treatment at all time points, strongly indicating that PHF8 overexpression induces a sustained EMT signaling program. mRNA profiles of MCF10A-Mock (control) and MCF10A-PHF8 with TGF-β1 treatment for 0, 24, 48 and 72 hours were generated by RNA-seq, in duplicate, using HiSeq2500 instrument.
2016-10-26 | E-GEOD-74377 | biostudies-arrayexpress
Project description:Basal-like breast cancers (BBC) exhibit subtype-specific phenotypic and transcriptional responses to stroma, but little research has addressed how stromal-epithelial interactions evolve during early BBC carcinogenesis. It is also unclear how common genetic defects, such as p53 mutations, modify these stromal-epithelial interactions. To address these knowledge gaps, we leveraged the MCF10 progression series of breast cell lines (MCF10A, MCF10AT1, and MCF10DCIS) to develop a longitudinal, tissue-contextualized model of p53-deficient, pre-malignant breast. Acinus asphericity, a morphogenetic correlate of cell invasive potential, was quantified with optical coherence tomography imaging, and gene expression microarrays were performed to identify transcriptional changes associated with p53 depletion and stromal context. Co-culture with stromal fibroblasts significantly increased the asphericity of acini derived from all three p53-deficient, but not p53-sufficient, cell lines, and was associated with the upregulation of 38 genes. When considered as a multigene score, these genes were upregulated in co-culture models of invasive BBC with increasing stromal content, as well as in basal-like relative to luminal breast cancers in two large human datasets. Taken together, stromal-epithelial interactions during early BBC carcinogenesis are dependent upon epithelial p53 status, and may play important roles in the acquisition of an invasive morphologic phenotype.
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Project description:PHF8 exerts distinct functions in different types of cancer. However, the mechanisms underlying its specific functions in each case remain obscure. To establish whether overexpression of PHF8 regulates the TGF-β induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-β1 for 0, 24, 48 and 72 hours and performed RNA-seq in biological duplicates. Our data indicated that EMT gene signatures were significantly enriched in MCF10A-PHF8 cells with TGF-β1 treatment at all time points, strongly indicating that PHF8 overexpression induces a sustained EMT signaling program.
2016-10-26 | GSE74377 | GEO
Project description:The HER2 (ERBB2) and MYC genes are commonly amplified genes in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self renewal and tumour propagating capability of cells transformed with Her2 and c-Myc. Co-expression of both oncogenes in cultured cells led to a pronounced activation of a c-Myc transcriptional signature and acquisition of a self renewing phenotype independent of an EMT programme or regulation of cancer stem cell markers. We show that HER2 and c-MYC are frequently co-amplified in a clinical breast cancer cohort and that co-amplification is strongly associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in patients receiving adjuvant chemotherapy (but not targeted anti-HER2 therapy), MYC amplification is associated with a poor outcome in HER2+ breast cancer patients. These findings demonstrate the importance of molecular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have important diagnostic and therapeutic consequences for the clinical management of HER2+ breast cancer. Gene expression analysis of Her2, Myc, and Her2 + Myc over expression on MCF10A cells, with MCF10A vector control comparison
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Project description:Excessive expression of subunit 1 of GIRK1 in ER+ breast tumors is associated with reduced survival times, and increased lymph node metastasis in patients. To investigate possible tumor-initiating properties, benign MCF10A and malign MCF7 mammary epithelial cells overexpressing GIRK1 were engineered, neoplasia associated vital parameters and resting potentials were measured and compared to controls. Presence of GIRK1 resulted in resting potentials negative to controls. Upon GIRK1 overexpression, several cellular pathways were sizably regulated towards pro-tumorigenic action as revealed by comparison of transcriptomes of MCF10AGIRK1 with control (MCF10AeGFP). According to transcriptome analysis, cellular migration was promoted while wound healing and extracellular matrix interactions were impaired. Vital parameters in MCF7 cells were affected akin the benign MCF10A lines, although to a lesser extent. Thus, GIRK1 overexpression will aid in classification of ER+ breast tumors and bears the potential to open a new window for the therapy of this detrimental disease.
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Project description:To study the biological and functional role of vimentin in maintenance of the mesenchymal phenotype of mammary epithelial cells, vimentin was silenced in the non-transformed MCF10A cells and vimentin-dependent changes in gene expression were analyzed.
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