ArticleCancer research2026
Chemotherapy-Treated Breast Cancer Cells Activate the WNT Signaling Pathway to Enter a Diapause-Like Early Persister State.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Decoding the metabolic cipher of dormant cancer cells: molecular mechanisms and therapeutic potentials.Cell communication and signaling : CCS · 2026Review
- Development and validation of an interpretable prognostic model for bladder cancer based on lactylation associated genes using SHAP analysis.Discover oncology · 2026Article
- A recurrently perturbed 12-gene program marks drug-tolerant persister states across cancer types.Frontiers in bioinformatics · 2026Article
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Authors and funding
24 authors.
Funding
Abstract
Cancer cells can acquire a reversible, dormant drug-tolerant persister state mimicking embryonic diapause to evade therapy pressure. Deciphering the precise mechanisms driving cancer cells into or out of a diapause-like persister cell state could provide strategies to overcome resistance. In this study, we showed that following chemotherapy, diverse therapeutic agents converge on WNT pathway activation to induce a de novo diapause-like cell state across various triple-negative breast cancer cell line, xenograft, and patient-derived organoid models. Among early persister cells, only transcriptionally WNT-active persisters exhibited the transcriptional and functional characteristics typical of diapause-like cells, including a negative correlation with MYC transcriptional activity and reversible restricted proliferation. The WNT signaling pathway functioned as both an inducer and biomarker of the diapause-like early persister cell state in both parental (chemotherapy-naïve) and chemotherapy-treated cells. Entry into and exit from the diapause-like early persister cell state was triggered by the transcriptional upregulation of components essential for canonical WNT ligand secretion. A combinatorial treatment strategy inhibiting WNT ligand secretion alongside chemotherapy effectively targeted the early mechanisms underlying the acquisition and enrichment of a diapause-like cell phenotype. These findings reveal WNT pathway activation as an early event that leads to a reversible diapause-like persister state and highlight the potential of targeting this axis to prevent the development of drug-resistant populations before they are firmly established. SIGNIFICANCE: WNT signaling is a crucial driver and biomarker of a reversible, dormant, diapause-like persister state in breast cancer cells, offering insights that could transform therapeutic strategies to disrupt tumor persistence.
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