ArticleProceedings of the National Academy of Sciences of the United States of America2025
Inflammation awakens dormant cancer cells by modulating the epithelial-mesenchymal phenotypic state.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Does acute inflammation triggered by infection promote cancer progression?PLoS biology · 2026Review
- Postoperative wound microenvironment regulates breast cancer stem cell fate and clinical implications.Molecular biology reports · 2026Review
- Tumor-Driven Inflammation Promotes Tumor Growth: A Focus on Anti-Inflammatory Cancer Treatments.Diseases (Basel, Switzerland) · 2026Review
- Article
- Targeting the Barriers Driving Immune Exclusion.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Intrinsic and extrinsic regulators of cancer dormancy and awakening.Journal of the National Cancer Center · 2026Review
- Ubiquitination of DDX21 by HERC2 induces a dormancy-like phenotype via the NUCKS1-p21/p27 axis to promote radio-resistance in colorectal cancer cells.Cell death & disease · 2026Article
- Regulating the dormancy of cancer stem cells: a novel approach to preventing cancer relapse.Cell death & disease · 2026Review
- Heat up and Destroy: Immunotherapy of "Cold" Tumors Using the Example of Glioblastoma.International journal of molecular sciences · 2026Review
- Neutrophil extracellular traps promote lung colonization of triple-negative breast cancer by inducing mesenchymal to epithelial transition.Frontiers in immunology · 2026Article
- Molecular and microenvironmental networks driving tumor dormancy: pathological mechanisms and emerging clinical strategies.Frontiers in medicine · 2026Review
- Inflammation awakens dormant cancer cells by modulating the epithelial-mesenchymal phenotypic state.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
37 authors.
Funding
Abstract
The awakening of dormant disseminated cancer cells appears to be responsible for the clinical relapses of patients whose primary tumors have been successfully cured months and even years earlier. In the present study, we demonstrate that dormant breast cancer cells lodged in the lungs reside in a highly mesenchymal, nonproliferative phenotypic state. The awakening of these cells is not triggered by a cancer cell-autonomous process. Instead, lung inflammation induced by the chemotherapeutic agent bleomycin effectively awakens dormant cancer cells, providing useful models for studying metastatic awakening. Mechanistically, the awakened cells shift from a highly mesenchymal to a quasi-mesenchymal phenotypic state in which they acquire tumorigenicity and proliferative ability. Once awakened, these cells can stably reside in this quasi-mesenchymal state and maintain their tumor-initiating ability, doing so without ongoing heterotypic signaling from the lung microenvironment. Epidermal growth factor receptor ligands released by the cells of the injured tissue microenvironment, including notably M2 type macrophages, promote dormant cancer cells to move toward this quasi-mesenchymal state, a transition that is critical for the awakening process. An understanding of the mechanisms of metastatic awakening may lead in the future to treatment strategies designed to prevent such awakening and resulting metastatic relapse.
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