ArticleJournal of extracellular vesicles2020
Triple knockdown of CDC37, HSP90-alpha and HSP90-beta diminishes extracellular vesicles-driven malignancy events and macrophage M2 polarization in oral cancer.
Article in Journal of extracellular vesicles, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 100 citations in OpenAlex.
- Extracellular Vesicles in Head and Neck Cancer-A Systematic Review.Journal of extracellular biology · 2026Review
- Salivary Extracellular Vesicles: Paradigm Shift in Liquid Biopsy Diagnostics.Journal of extracellular biology · 2026Review
- HSP90B1 facilitates glioma radiotherapy resistance by regulating RhoC ubiquitin‒proteasome degradation.Genes & diseases · 2026Article
- Identification of Bruceine A as a novel HSP90AB1 inhibitor for suppressing hepatocellular carcinoma growth.Journal of advanced research · 2026Article
- MMP-3 cleavage of Lamin A induces pro-migratory nuclear deformity, nucleophagy, and their autophagic secretion with extracellular vesicles in metastatic cancer.Cell communication and signaling : CCS · 2026Article
- ATPase copper transporting beta contributes to cisplatin resistance as a regulatory factor of extracellular vesicles in head and neck squamous cell carcinoma.Cancer gene therapy · 2026Article
- Review
- Adipose Tissue Macrophages as Initiators of Exacerbated Periodontitis in Estrogen-Deficient Environments via the Amplifier Extracellular Vesicles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Extracellular Vesicles for Clinical Diagnostics: From Bulk Measurements to Single-Vesicle Analysis.ACS nano · 2025Review
- Role of M2 macrophage-derived exosomes in cancer drug resistance via noncoding RNAs.Discover oncology · 2025Review
- Natural and Bioengineered Extracellular Vesicles in Diagnosis, Monitoring and Treatment of Cancer.ACS nano · 2025Review
- Prospect of extracellular vesicles in tumor immunotherapy.Frontiers in immunology · 2025Review
- A new weapon: the application of tumor vaccines based on extracellular exosomal heat shock proteins in immunotherapy.Frontiers in immunology · 2025Review
- Immunomodulatory effects of photothermal therapy in breast cancer: advances and challenges.Frontiers in immunology · 2025Review
- Schwann cell-secreted frizzled-related protein 1 dictates neuroinflammation and peripheral nerve degeneration after neurotrauma.Cell reports. Medicine · 2024Article
- Extracellular heat shock protein 90 alpha (eHsp90α)'s role in cancer progression and the development of therapeutic strategies.European journal of medicinal chemistry · 2024Review
- Hsp90α and cell death in cancers: a review.Discover oncology · 2024Review
- Stress biology: Complexity and multifariousness in health and disease.Cell stress & chaperones · 2024Article
- Tumour-associated macrophage-derived DOCK7-enriched extracellular vesicles drive tumour metastasis in colorectal cancer via the RAC1/ABCA1 axis.Clinical and translational medicine · 2024Article
- Emerging roles of exosomes in oral diseases progression.International journal of oral science · 2024Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence has been accumulating to indicate that extracellular vesicles (EVs), including exosomes, released by cancer cells can foster tumour progression. The molecular chaperones - CDC37, HSP90α and HSP90β play key roles in cancer progression including epithelial-mesenchymal transition (EMT), although their contribution to EVs-mediated cell-cell communication in tumour microenvironment has not been thoroughly examined. Here we show that triple depletion of the chaperone trio attenuates numerous cancer malignancy events exerted through EV release. Metastatic oral cancer-derived EVs (MEV) were enriched with HSP90α HSP90β and cancer-initiating cell marker CD326/EpCAM. Depletion of these chaperones individually induced compensatory increases in the other chaperones, whereas triple siRNA targeting of these molecules markedly diminished the levels of the chaperone trio and attenuated EMT. MEV were potent agents in initiating EMT in normal epithelial cells, a process that was attenuated by the triple chaperone depletion. The migration, invasion, and in vitro tumour initiation of oral cancer cells were significantly promoted by MEV, while triple depletion of CDC37/HSP90α/β reversed these MEV-driven malignancy events. In metastatic oral cancer patient-derived tumours, HSP90β was significantly accumulated in infiltrating tumour-associated macrophages (TAM) as compared to lower grade oral cancer cases. HSP90-enriched MEV-induced TAM polarization to an M2 phenotype, a transition known to support cancer progression, whereas the triple chaperone depletion attenuated this effect. Mechanistically, the triple chaperone depletion in metastatic oral cancer cells effectively reduced MEV transmission into macrophages. Hence, siRNA-mediated knockdown of the chaperone trio (CDC37/HSP90α/HSP90β) could potentially be a novel therapeutic strategy to attenuate several EV-driven malignancy events in the tumour microenvironment. ABBREVIATIONS: CDC37: cell division control 37; EMT: epithelial-mesenchymal transmission; EV: extracellular vesicles; HNSCC: head and neck squamous cell carcinoma; HSP90: heat shock protein 90; TAM: tumour-associated macrophage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.