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Effect of tet-inducible expression of individual MAP3Ks (COT, MEKK1, MEKK2, MEKK3, ASK1, ASK3, ARAF, RAF1, BRAF, NIK, ZAK1, MLK3, MLK1) in MCF10A mammary epithelial cells.

ABSTRACT: To investigate the cooperative function ERK, JNK and p38 signaling in cell behavior decisions, we established MCF10A cell lines in which each target gene has been overexpressed by stable integration of a TRE3G (TET) inducible promoter driver the expression of each target gene. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 independent repliatse at 18 hours post induction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213882 | GEO | 2022/09/26

REPOSITORIES: GEO

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Effect of tet-inducible expression of individual MAP3Ks (COT, MEKK1, MEKK2, MEKK3, ASK1, ASK3, ARAF, RAF1, BRAF, NIK, ZAK1, MLK3, MLK1) in MCF10A mammary epithelial cells.

Project description:Effect of tet-inducible expression of individual MAP3Ks (COT, MEKK1, MEKK2, MEKK3, ASK1, ASK3, ARAF, RAF1, BRAF, NIK, ZAK1, MLK3, MLK1) in MCF10A mammary epithelial cells.

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Genomic binding of RUNX1 in MCF10A cells

Project description:The overall goal of this study is to identify the genomic binding of RUNX1 in MCF10A cells. We used ChIPseq (chromatin immunoprecipitation assay followed by deep sequencing) to identify the binding sites of RUNX1 in MCF10A cells. We performed ChIPseq of RUNX1 using parental MCF10A cells and did not identify high confident binding sites. To overcome this hurdle, we first generated a RUNX1 deleted MCF10A cell line using CRISPR-Cas9. We then transduced this RUNX1 KO MCF10A cells with lentiviruses that inducibly expresses RUNX1. After treating RUNX1 inducible MCF10A cells with 1 ug/ml doxycycline for 24 hours, we performed ChIPseq of RUNX1.

2019-04-18 | GSE129314 | GEO

Overexpression of PHF8 promotes an EMT-related gene signature in MCF10A cells

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

Targetable BRAF and RAF1 Alterations in Advanced Pediatric Cancers.

Project description:RAF family protein kinases signal through the MAPK pathway to orchestrate cellular proliferation, survival, and transformation. Identifying BRAF alterations in pediatric cancers is critically important as therapeutic agents targeting BRAF or MEK may be incorporated into the clinical management of these patients. In this study, we performed comprehensive genomic profiling on 3,633 pediatric cancer samples and identified a cohort of 221 (6.1%) cases with known or novel alterations in BRAF or RAF1 detected in extracranial solid tumors, brain tumors, or hematological malignancies. Eighty percent (176/221) of these tumors had a known-activating short variant (98, 55.7%), fusion (72, 40.9%), or insertion/deletion (6, 3.4%). Among BRAF altered cancers, the most common tumor types were brain tumors (74.4%), solid tumors (10.8%), hematological malignancies (9.1%), sarcomas (3.4%), and extracranial embryonal tumors (2.3%). RAF1 fusions containing intact RAF1 kinase domain (encoded by exons 10-17) were identified in seven tumors, including two novel fusions TMF1-RAF1 and SOX6-RAF1. Additionally, we highlight a subset of patients with brain tumor with positive clinical response to BRAF inhibitors, demonstrating the rationale for incorporating precision medicine into pediatric oncology. IMPLICATIONS FOR PRACTICE: Precision medicine has not yet gained a strong foothold in pediatric cancers. This study describes the landscape of BRAF and RAF1 genomic alterations across a diverse spectrum of pediatric cancers, primarily brain tumors, but also encompassing melanoma, sarcoma, several types of hematologic malignancy, and others. Given the availability of multiple U.S. Food and Drug Administration-approved BRAF inhibitors, identification of these alterations may assist with treatment decision making, as described here in three cases of pediatric cancer.

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Interactome dynamics of RAF1-BRAF kinase monomers and dimers.

Project description:RAF kinases play major roles in cancer. BRAFV600E mutants drive ~6% of human cancers. Potent kinase inhibitors exist but show variable effects in different cancer types, sometimes even inducing paradoxical RAF kinase activation. Both paradoxical activation and drug resistance are frequently due to enhanced dimerization between RAF1 and BRAF, which maintains or restores the activity of the downstream MEK-ERK pathway. Here, using quantitative proteomics we mapped the interactomes of RAF1 monomers, RAF1-BRAF and RAF1-BRAFV600E dimers identifying and quantifying >1,000 proteins. In addition, we examined the effects of vemurafenib and sorafenib, two different types of clinically used RAF inhibitors. Using regression analysis to compare different conditions we found a large overlapping core interactome but also distinct condition specific differences. Given that RAF proteins have kinase independent functions such dynamic interactome changes could contribute to their functional diversification. Analysing this dataset may provide a deeper understanding of RAF signalling and mechanisms of resistance to RAF inhibitors.

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Activating NRF1-BRAF and ATG7-RAF1 fusions in anaplastic pleomorphic xanthoastrocytoma without BRAF p.V600E mutation.

Project description: Not available

| S-EPMC5074852 | biostudies-literature

HOXA5 depletion in MCF10A cells

Project description:Microarray analysis of gene expression in MCF10A cells following HOXA5 depletion.

2016-02-01 | GSE75840 | GEO

Overexpression of PHF8 promotes an EMT-related gene signature in MCF10A cells

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-Î² induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-Î²1 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-Î²1 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-Î²1 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

Gene Expression in MCF10A cells through Differentiation on Transwells

Project description:To further understand the differences occurring in MCF10A cells as they polarize and differentiate in the TranswellÂ® model, we performed gene expression profiling with Affymetrix Human Genome U133 Plus 2.0 Arrays. Four experimental time points, were sampled: conventional cultures of MCF10A cells grown on plastic (Monolayer) and MCF10A cells plated on TranswellsÂ® sampled at three TEER values, 200-300 Î© cm2 (Base), 1400-1600 Î© cm2 (Midpoint), and 3000-3200 Î© cm2 (Plateau). Experiment Overall Design: Cells are grown in monolayer to 90-95% confluency, trypsinized and counted for seeding onto permeable supports (TranswellÂ®, 0.4 Âµm pores, polyester) in normal growth medium. MCF10A cells are seeded on 12-well TranswellsÂ® (Corning) at 105 cells/cm2. Both chambers of media were changed strictly on a 24-hour schedule. Transepithelial electrical resistance (TEER) is measured daily with Epithelial Volt-Ohm Meter (EVOM; World Precision Instruments), prior to media change. Total RNA was isolated at the indicated TEER listed above. Canonical monolayer MCF10A cells served as a control comparison. Each time point was performed on triplicate arrays except for Plateau (n=4).

2008-06-11 | E-GEOD-10070 | biostudies-arrayexpress

Time course microarray data following GR activation in MCF10A-Myc breast cells

Project description:This series contain time course microarray data from MCF10A-Myc cells treated with either ethanol or Dexamethasone for 30 min, 2 hr, 4 hr, and 24 hr. This series contains three biological replicates that were analyzed as independent replicate experiments (data were normalized within each replicate experiment, not across all samples). Keywords: time course

2006-06-02 | GSE4917 | GEO

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