The cancer-associated cell migration protein TSPAN1 is under control of androgens and its upregulation increases prostate cancer cell migration


Munkley, Jennifer, McClurg, Urszula L ORCID: 0000-0003-2631-4174, Livermore, Karen E, Ehrmann, Ingrid, Knight, Bridget, Mccullagh, Paul, Mcgrath, John, Crundwell, Malcolm, Harries, Lorna W, Leung, Hing Y et al (show 4 more authors) (2017) The cancer-associated cell migration protein TSPAN1 is under control of androgens and its upregulation increases prostate cancer cell migration. SCIENTIFIC REPORTS, 7 (1). 5249-. ISSN 2045-2322, 2045-2322

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Abstract

Cell migration drives cell invasion and metastatic progression in prostate cancer and is a major cause of mortality and morbidity. However the mechanisms driving cell migration in prostate cancer patients are not fully understood. We previously identified the cancer-associated cell migration protein Tetraspanin 1 (TSPAN1) as a clinically relevant androgen regulated target in prostate cancer. Here we find that TSPAN1 is acutely induced by androgens, and is significantly upregulated in prostate cancer relative to both normal prostate tissue and benign prostate hyperplasia (BPH). We also show for the first time, that TSPAN1 expression in prostate cancer cells controls the expression of key proteins involved in cell migration. Stable upregulation of TSPAN1 in both DU145 and PC3 cells significantly increased cell migration and induced the expression of the mesenchymal markers SLUG and ARF6. Our data suggest TSPAN1 is an androgen-driven contributor to cell survival and motility in prostate cancer.

Item Type: Article
Uncontrolled Keywords: Tumor Cells, Cultured, Humans, Prostatic Neoplasms, Prostatic Hyperplasia, Androgens, Prognosis, Case-Control Studies, Follow-Up Studies, Apoptosis, Cell Proliferation, Cell Movement, Gene Expression Regulation, Neoplastic, Male, Epithelial-Mesenchymal Transition, Tetraspanins, Biomarkers, Tumor
Depositing User: Symplectic Admin
Date Deposited: 06 Nov 2018 12:46
Last Modified: 07 Dec 2024 20:07
DOI: 10.1038/s41598-017-05489-5
Related URLs:
URI: https://livrepository.liverpool.ac.uk/id/eprint/3028463
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