Next Generation Sequencing (RNA-Sequencing) for the analysis of RUNX3 and YAP1 targets in TGFb-stimulated HEK 293 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE226590 | GEO | 2023/11/09
REPOSITORIES: GEO
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Project description:Comparision of the gene expression profiles of the RUNX3 Knock out and RUNX3 restored cells.
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Project description:Next Generation Sequencing (RNA-Sequencing) for the analysis of RUNX3 and YAP1 targets in TGFb-stimulated HEK 293 cells
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Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA
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2013-11-18 | E-GEOD-50123 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to compare the gene expression profiles of H460, H460-ERT2-RUNX3-WT and H460-ERT2-RUNX3-MT(K94/171R) cells. Methods: H460, H460-ERT2-RUNX3 WT, and H460-ERT2-RUNX3-MT(K94/171R) cells were serum-starved for 24 hr, and then stimulated with 10% serum or 10% serum + 1 uM 4-OHT for 0, 8, or 16 hr. RNA was extracted from the cells. Isolated total RNA was processed for preparation of an RNA-seq library using the Illumina TruSeq Stranded mRNA Sample Preparation kit (Illumina, San Diego, CA, USA). Quality and size of libraries were assessed using the Agilent 2100 Bioanalyzer DNA kit (Agilent, Santa Clara, CA, USA). All libraries were quantified by qPCR using a CFX96 Real Time System (Bio-Rad, Hercules, CA, USA) and sequenced on NextSeq500 sequencers (Illumina). Sequencing adapters and low-quality bases in the raw reads were trimmed using the Cutadapt software. The cleaned high-quality reads were mapped to the human reference genome hg19 (https://genome.ucsc.edu) using STAR software. Genes differentially expressed between two selected biological conditions were identified by Cuffdiff in the Cufflinks package (http://cole-trapnell-lab.github.io/cufflinks/papers/). Results: RNA-Sequencing Data suggest that the R-point defends against oncogenic K-RAS–induced tumorigenesis not only by regulating intracellular programs (cell cycle, apoptosis, and metabolic pathways), but also by regulating extracellular programs (inflammatory response and immune response).
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Project description:Murine Runx3 is expressed in developing bone osteoblasts (OBLs) and its deletion in these cells culminates in severe congenital osteopenia. We demonstrate that Runx3 is non-redundantly involved in the proliferation of early pre-committed OBL progenitor cells, a critical step in the generation of adequate numbers of bone-forming OBLs. Thus, in the absence of Runx3 in cells of this lineage, the number of mature/active OBLs is significantly diminished, providing a mechanistic explanation to the observed osteopenia. This experiment was aimed at identifying genes that are likely regulated by Runx3 along osteoblastogenesis. To elucidate the Runx3-mediated transcriptional program along OBL differentiation, we compared gene expression profile in WT and Runx3f/f/Col1a1-cre calvarial OBLs. Progenitor cells were purified and RNA extracted, reverse-transcribed, fragmented, labeled and hybridized to GeneChip® Mouse Gene 2.0 ST Array.
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Project description:Cholesterol is one of the major lipid components of the plasma membrane in mammalian cells and is involved in the regulation of a number of ion channels. The present study investigates how large conductance Ca(2+)-activated K(+) (BK) channels are regulated by membrane cholesterol in BK-HEK 293 cells expressing both the ?-subunit hKCa1.1 and the auxiliary ?1-subunit or in hKCa1.1-HEK 293 cells expressing only the ?-subunit hKCa1.1 using approaches of electrophysiology, molecular biology, and immunocytochemistry. Membrane cholesterol was depleted in these cells with methyl-?-cyclodextrin (M?CD), and enriched with cholesterol-saturated M?CD (M?CD-cholesterol) or low-density lipoprotein (LDL). We found that BK current density was decreased by cholesterol enrichment in BK-HEK 293 cells, with a reduced expression of KCa1.1 protein, but not the ?1-subunit protein. This effect was fully countered by the proteasome inhibitor lactacystin or the lysosome function inhibitor bafilomycin A1. Interestingly, in hKCa1.1-HEK 293 cells, the current density was not affected by cholesterol enrichment, but directly decreased by M?CD, suggesting that the down-regulation of BK channels by cholesterol depends on the auxiliary ?1-subunit. The reduced KCa1.1 channel protein expression was also observed in cultured human coronary artery smooth muscle cells with cholesterol enrichment using M?CD-cholesterol or LDL. These results demonstrate the novel information that cholesterol down-regulates BK channels by reducing KCa1.1 protein expression via increasing the channel protein degradation, and the effect is dependent on the auxiliary ?1-subunit.
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