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Gene expression signatures of MDCK-pTR GFP-RasV12 cells cultured alone or mixed with MDCK cells

ABSTRACT: Gene expression signatures of MDCK-pTR GFP-RasV12 cells cultured alone or mixed with MDCK cells

PROVIDER: PRJNA991983 | ENA |

REPOSITORIES: ENA

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Gene expression of normal MDCK cells mixed with normal MDCK cells or RasV12-transformed MDCK cells

Project description:To investigate whether and how the presence of RasV12-transformed cells influences the gene expression profile of the neighbouring normal epithelial cells, we performed microarray analysis. Normal Madin-Darby canine kidney (MDCK) cells were co-cultured with MDCK cells expressing GFP or GFP-RasV12. GFP-negative normal MDCK cells were then collected by FACS, and expression of various genes was compared between the two conditions.

2020-03-10 | E-MTAB-8769 | biostudies-arrayexpress

Gene expression signatures of MDCK-pTR GFP-RasV12 mCherry-β-catenin Δ131 cells cultured alone or mixed with MDCK mCherry-β-catenin Δ131 cells

Project description:Gene expression signatures of MDCK-pTR GFP-RasV12 mCherry-β-catenin Δ131 cells cultured alone or mixed with MDCK mCherry-β-catenin Δ131 cells

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Gene expression signatures of MDCK-pTR GFP-RasV12 cells cultured alone or mixed with MDCK cells

Project description:Newly emerging transformed cells carrying genetic defects, including the active Ras mutant, are apicall extruded when surrounded by normal epithelial cells. This biological phenomenon is termed as cell competition. It remains elusive which factors prime RasV12-transformed cells to be expelled via cell competition. Here, We performe microarray analysis to search for molecules whose expression is changed in RasV12 cells surrounded by normal cells.

2023-07-11 | GSE236658 | GEO

Gene expression signatures of MDCK-pTR GFP-RasV12 mCherry-β-catenin Δ131 cells cultured alone or mixed with MDCK mCherry-β-catenin Δ131 cells

Project description:Normal epithelial cells exert their competitive advantage over RasV12-transformed cells and eliminate them into apical lumen via cell competition. However, it remains elusive which internal or external factors compromise cell competition and provoke oncogenesis. Here, we examine the effect of sequential accumulation of gene mutations mimicking multi-sequential carcinogenesis on RasV12-induced cell competition. Consequently, we find that directionality of cell extrusion of RasV12 cells mosaically produced within Wnt-activated epithelia is reversed, and transformed cells are delaminated into basal lamina via non-cell autonomous MMP21 upregulation. Elevated production of MMP21 is elicited partly through NF-κB signaling, which blockage restores apical elimination of RasV12 cells. Collectively, this study demonstrates that cells with high mutational burdens exploit cell competition for their benefit by behaving as unfit cells and are endowed with an invasion advantage. We performed microarray analysis to search for molecules whose expression is changed in β-catenin Δ131/RasV12 cells surrounded by β-catenin Δ131 cells.

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Project description:We engineered KSR1-/- mouse embryonic fibroblasts (MEFs) to express GFP alone, KSR1 or RasV12 and GFP, or KSR1, H-RasV12 and GFP, and performed gene expression profiling on all 4 cell lines. Each cell line was measured in triplicate: 1. GFP alone 2. H-RasV12 and GFP 3. KSR1 and GFP 4. KSR1, H-RasV12, and GFP

2011-04-02 | E-GEOD-28228 | biostudies-arrayexpress

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2015-10-20 | GSE68989 | GEO

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Project description:RNAseq of GFP-sorted cells (Low-GFP vs. High-GFP, GFP-fed vs GFP+fed)

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