ArticleBritish journal of cancer2025
Wnt/ERK/CDK4/6 activation in the partial EMT state coordinates mammary cancer stemness with self-renewal and inhibition of differentiation.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Article
- CD44 knockdown and TGF‑β inhibition modulate cell proliferation and invasion in claudin‑low breast cancer cells.Oncology reports · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
backgroundThe hybrid EMT state is a key driver of tumour regenerative and metastatic potential; however, the mechanism whereby this programme regulates tumour stemness with respect to self-renewal and differentiation remains unclear.
methodsWe isolated epithelial/mesenchymal (E/M) (CD104
resultsE/M cells were endowed with organoid-forming ability as well as by tumour-initiating and metastatic potential relative to M cells. Interestingly, Wnt3a stimulates transient ERK/CDK4/6 activation in E/M cells, thereby upregulating FOXC2, and in turn TAp63 and ΔNp63, which support the hybrid state. In parallel, ERK/CDK4/6 activates S-phase and FOXM1, thereby promoting self-renewal. Remarkably, transient ERK activation by Wnt3a deactivates EGFR, thus preventing sustained ERK phosphorylation from causing E/M differentiation. Consistently, ERK/CDK4/6 drug perturbation in E/M cells suppressed FOXC2/p63, FOXM1, self-renewal, organoid formation and mammary tumour growth via epithelial differentiation.
conclusionsThese findings unravelled a mechanism whereby the hybrid EMT state regulates stemness, self-renewal and differentiation via transient Wnt/ERK/CDK4/6 activation, which can be leveraged for cancer stem cell therapy.
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