ArticleInternational journal of molecular sciences2020
Fluid Shear Stress Induces EMT of Circulating Tumor Cells via JNK Signaling in Favor of Their Survival during Hematogenous Dissemination.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Mechanobiology of solid tumor vasculature: implications for tumor progression.Cancer metastasis reviews · 2026Review
- Mechanoadaptation via Myosin Cytoplasmic Redistribution Protects Circulating Tumor Cells From Shear-induced Death During Hematogenous Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nuclear Mechanotransduction Across the Metastatic Cascade: Decoding Spatiotemporal Heterogeneity in Cancer Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Roles of cytoskeleton in metastasis: from its mechanism to therapeutic strategies.Experimental & molecular medicine · 2026Review
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- Review
- Cancer cells metastasize in several types of cancer via two distinct routes, probably based on mechanical signals.Frontiers in cell and developmental biology · 2026Review
- Ezrin Functions as a Key Mechanosensitive Effector to Preserve Cell Structure and Promote Survival and Metastasis of Lung Cancer Cells during Circulation.International journal of biological sciences · 2026Article
- The phenotypic heterogeneity of tumor-derived cells in the bloodstream of pancreatic cancer patients.Frontiers in cell and developmental biology · 2026Article
- Biophysical adaptations of circulating tumor cells undergoing metastasis.Biophysics reports · 2025Article
- Circulating Tumor Cells for the Monitoring of Lung Cancer Therapies.International journal of molecular sciences · 2025Review
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- Review
- Correlation of radiotherapy, targeted therapy, and immunotherapy with hepatocellular carcinoma recurrence.World journal of gastrointestinal oncology · 2025Review
- Integrating model systems and genomic insights to decipher mechanisms of cancer metastasis.Nature reviews. Genetics · 2025Review
- Circulating Tumor Microenvironment in Metastasis.Cancer research · 2025Review
- Focus on mechano-immunology: new direction in cancer treatment.International journal of surgery (London, England) · 2025Review
- Research progress on mechanisms of tumor immune microenvironment and gastrointestinal resistance to immunotherapy: mini review.Frontiers in immunology · 2025Review
- Decoding Metastasis: From Cell Death to Fusion in Cancer Progression.Current cancer drug targets · 2025Review
- Analysis of the Plasticity of Circulating Tumor Cells Reveals Differentially Regulated Kinases During the Suspension-to-Adherent Transition.Cancer medicine · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells metastasize to distal organs mainly through hematogenous dissemination, where they experience considerable levels of fluid shear stress. Epithelial-mesenchymal transition (EMT) plays a critical role in tumor metastasis. However, how fluid shear stress influences the EMT phenotype of circulating tumor cells (CTCs) in suspension has not been fully understood. The role of shear-induced EMT in cell survival under blood shear flow remains unclear. This study shows that the majority of breast CTCs underwent apoptosis under shear flow and the surviving cells exhibited mesenchymal phenotype, suggesting that fluid shear stress induces EMT. Mechanistically, fluid shear stress-activated Jun N-terminal kinase (JNK) signaling, inhibition/activation of which suppressed/promoted the EMT phenotype. In particular, shear flow facilitated the JNK-dependent transition of epithelial CTCs into the mesenchymal status and maintained the pre-existing mesenchymal cells. Importantly, the induction of EMT suppressed the pro-apoptosis gene p53 upregulated modulator of apoptosis (PUMA) and enhanced the survival of suspended CTCs in fluid shear stress, which was rescued by overexpressing PUMA or silencing JNK signaling, suggesting that shear-induced EMT promotes CTC survival through PUMA downregulation and JNK activation. Further, the expressions of EMT markers and JUN were correlated with poor patient survival. In summary, our findings have demonstrated that fluid shear stress induces EMT in suspended CTCs via JNK signaling that promotes their survival in shear flow. This study thus unveils a new role of blood shear stress in CTC survival and facilitates the development of novel therapeutics against tumor metastasis.
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