INVITED RESEARCH HIGHLIGHT
Year : 2014  |  Volume : 16  |  Issue : 4  |  Page : 530-535

Trading in your spindles for blebs: the amoeboid tumor cell phenotype in prostate cancer


1 Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, and The Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Urological Diseases Research Center, Boston Children's Hospital and Department of Surgery, Harvard Medical School, Boston, MA, USA
2 Urological Diseases Research Center, Boston Children's Hospital; Department of Surgery, Harvard Medical School, Boston, MA, USA
3 Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, and The Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA
4 Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, and The Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Urological Diseases Research Center, Boston Children's Hospital; Department of Surgery, Harvard Medical School, Boston, MA and Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA

Correspondence Address:
Dolores Di Vizio
Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, and The Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Urological Diseases Research Center, Boston Children's Hospital and Department of Surgery, Harvard Medical School, Boston, MA
USA
Michael R Freeman
Division of Cancer Biology and Therapeutics, Departments of Surgery, Medicine and Biomedical Sciences, and The Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA; Urological Diseases Research Center, Boston Children's Hospital; Department of Surgery, Harvard Medical School, Boston, MA and Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1008-682X.122877

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Prostate cancer (PCa) remains a principal cause of mortality in developed countries. Because no clinical interventions overcome resistance to androgen ablation therapy, management of castration resistance and metastatic disease remains largely untreatable. Metastasis is a multistep process in which tumor cells lose cell-cell contacts, egress from the primary tumor, intravasate, survive shear stress within the vasculature and extravasate into tissues to colonize ectopic sites. Tumor cells reestablish migratory behaviors employed during nonneoplastic processes such as embryonic development, leukocyte trafficking and wound healing. While mesenchymal motility is an established paradigm of dissemination, an alternate, 'amoeboid' phenotype is increasingly appreciated as relevant to human cancer. Here we discuss characteristics and pathways underlying the phenotype, and highlight our findings that the cytoskeletal regulator DIAPH3 governs the mesenchymal-amoeboid transition. We also describe our identification of a new class of tumor-derived microvesicles, large oncosomes, produced by amoeboid cells and with potential clinical utility in prostate and other cancers.


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