Journal
MOLECULAR ONCOLOGY
Volume 7, Issue 6, Pages 1019-1030Publisher
WILEY
DOI: 10.1016/j.molonc.2013.07.008
Keywords
Prostate cancer; Gene expression signature; Meta-analysis; Metastasis; SPARCL1 function in vivo
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Funding
- Howard Temin Award from the National Cancer Institute at the National Institutes of Health [CA114033]
- American Cancer Society-Institutional Research Grant [IRG-58-009-51, IRG-58-009-53]
- Vanderbilt Clinical and Translational Science Awards (CTSA) from National Center for Research Resources (NCRR), a part of the National Institutes of Health (NIH) [UL1 RR024975, CRC1838]
- National Cancer Institute [4R01-CA076142-14]
- American Cancer Society Great Lakes Division-Michigan Cancer Research Fund Postdoctoral Fellowship
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Purpose: Metastasis, the main cause of death from cancer, remains poorly understood at the molecular level. Experimental design: Based on a pattern of reduced expression in human prostate cancer tissues and tumor cell lines, a candidate suppressor gene (SPARCL1) was identified. We used in vitro approaches to determine whether overexpression of SPARCL1 affects cell growth, migration, and invasiveness. We then employed xenograft mouse models to analyze the impact of SPARCL1 on prostate cancer cell growth and metastasis in vivo. Results: SPARCL1 expression did not inhibit tumor cell proliferation in vitro. By contrast, SPARCL1 did suppress tumor cell migration and invasiveness in vitro and tumor metastatic growth in vivo, conferring improved survival in xenograft mouse models. Conclusions: We present the first in vivo data suggesting that SPARCL1 suppresses metastasis of prostate cancer. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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