ArticleResearch square2026
Fluctuating environment causes neoplastic transition and epithelial-mesenchymal plasticity in human cells.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
Funding
Abstract
How environmental selective pressures contribute to the emergence of a neoplastic tumorigenic state, remains incompletely understood. Here we show that the immortalized non-tumorigenic breast epithelial cell line (MCF10A) develops neoplastic clones under fluctuating conditions in-vitro that mimic the harsh tumor microenvironment. Long-term evolutionary experiments and genomic landscape analyses of the clones identified ROS as the dominant clonal mutational signature that facilitates the acquisition of oncogenic driver mutations and the onset of the Warburg phenotype. Single cell multi-omics and brightfield microscopy further elucidate that each clone adopts two plastic phenotypic states, epithelial-like and mesenchymal-like, the transition between which is epigenetically mediated by de novo expression of Grainyhead-like Transcription Factor 2 (
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