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

ABSTRACT: 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.

ORGANISM(S): Canis lupus familiaris

PROVIDER: GSE217830 | GEO | 2022/11/16

REPOSITORIES: GEO

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

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