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- W4313557154 abstract "Phenotypic plasticity associated with the hybrid epithelial–mesenchymal transition (EMT) is crucial to metastatic seeding and outgrowth. However, the mechanisms governing the hybrid EMT state remain poorly defined. Here we showed that deletion of the epigenetic regulator MLL3, a tumour suppressor frequently altered in human cancer, promoted the acquisition of hybrid EMT in breast cancer cells. Distinct from other EMT regulators that mediate only unidirectional changes, MLL3 loss enhanced responses to stimuli inducing EMT and mesenchymal–epithelial transition in epithelial and mesenchymal cells, respectively. Consequently, MLL3 loss greatly increased metastasis by enhancing metastatic colonization. Mechanistically, MLL3 loss led to increased IFNγ signalling, which contributed to the induction of hybrid EMT cells and enhanced metastatic capacity. Furthermore, BET inhibition effectively suppressed the growth of MLL3-mutant primary tumours and metastases. These results uncovered MLL3 mutation as a key driver of hybrid EMT and metastasis in breast cancer that could be targeted therapeutically. Cui et al. identify an important role for MLL3 in regulating the hybrid epithelial–mesenchymal transition state in breast cancer and show that deletion of MLL3 enhances metastatic capacity through increased IFNγ signalling." @default.
- W4313557154 created "2023-01-06" @default.
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- W4313557154 date "2023-01-01" @default.
- W4313557154 modified "2023-09-29" @default.
- W4313557154 title "MLL3 loss drives metastasis by promoting a hybrid epithelial–mesenchymal transition state" @default.
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- W4313557154 doi "https://doi.org/10.1038/s41556-022-01045-0" @default.
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