SPARCL1 suppresses metastasis in prostate cancer

Yuzhu Xiang; Qingchao Qiu; Ming Jiang; Renjie Jin; Brian D. Lehmann; Douglas W. Strand; Bojana Jovanovic; David J. DeGraff; Yi Zheng; Dina A. Yousif; Christine Q. Simmons; Thomas C. Case; Jia Yi; Justin M. Cates; John Virostko; Xiusheng He; Xunbo Jin; Simon W. Hayward; Robert J. Matusik; AlfredL George; Yajun Yi

doi:10.1016/j.molonc.2013.07.008

SPARCL1 suppresses metastasis in prostate cancer

Yuzhu Xiang, Qingchao Qiu, Ming Jiang, Renjie Jin, Brian D. Lehmann, Douglas W. Strand, Bojana Jovanovic, David J. DeGraff, Yi Zheng, Dina A. Yousif, Christine Q. Simmons, Thomas C. Case, Jia Yi, Justin M. Cates, John Virostko, Xiusheng He, Xunbo Jin, Simon W. Hayward, Robert J. Matusik, AlfredL GeorgeYajun Yi

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

Abstract

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 invitro 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 invivo. Results: SPARCL1 expression did not inhibit tumor cell proliferation invitro. By contrast, SPARCL1 did suppress tumor cell migration and invasiveness invitro and tumor metastatic growth invivo, conferring improved survival in xenograft mouse models. Conclusions: We present the first invivo data suggesting that SPARCL1 suppresses metastasis of prostate cancer.

Original language	English (US)
Pages (from-to)	1019-1030
Number of pages	12
Journal	Molecular oncology
Volume	7
Issue number	6
DOIs	https://doi.org/10.1016/j.molonc.2013.07.008
State	Published - Dec 2013

Keywords

Gene expression signature
Meta-analysis
Metastasis
Prostate cancer
SPARCL1 function invivo

ASJC Scopus subject areas

Genetics
Molecular Medicine
Oncology
Cancer Research

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10.1016/j.molonc.2013.07.008

Cite this

Xiang, Y., Qiu, Q., Jiang, M., Jin, R., Lehmann, B. D., Strand, D. W., Jovanovic, B., DeGraff, D. J., Zheng, Y., Yousif, D. A., Simmons, C. Q., Case, T. C., Yi, J., Cates, J. M., Virostko, J., He, X., Jin, X., Hayward, S. W., Matusik, R. J., ... Yi, Y. (2013). SPARCL1 suppresses metastasis in prostate cancer. Molecular oncology, 7(6), 1019-1030. https://doi.org/10.1016/j.molonc.2013.07.008

Xiang, Y, Qiu, Q, Jiang, M, Jin, R, Lehmann, BD, Strand, DW, Jovanovic, B, DeGraff, DJ, Zheng, Y, Yousif, DA, Simmons, CQ, Case, TC, Yi, J, Cates, JM, Virostko, J, He, X, Jin, X, Hayward, SW, Matusik, RJ, George, A & Yi, Y 2013, 'SPARCL1 suppresses metastasis in prostate cancer', Molecular oncology, vol. 7, no. 6, pp. 1019-1030. https://doi.org/10.1016/j.molonc.2013.07.008

@article{71e067893bc84a1a855d2e2cc0911760,

title = "SPARCL1 suppresses metastasis in prostate cancer",

abstract = "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 invitro 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 invivo. Results: SPARCL1 expression did not inhibit tumor cell proliferation invitro. By contrast, SPARCL1 did suppress tumor cell migration and invasiveness invitro and tumor metastatic growth invivo, conferring improved survival in xenograft mouse models. Conclusions: We present the first invivo data suggesting that SPARCL1 suppresses metastasis of prostate cancer.",

keywords = "Gene expression signature, Meta-analysis, Metastasis, Prostate cancer, SPARCL1 function invivo",

author = "Yuzhu Xiang and Qingchao Qiu and Ming Jiang and Renjie Jin and Lehmann, {Brian D.} and Strand, {Douglas W.} and Bojana Jovanovic and DeGraff, {David J.} and Yi Zheng and Yousif, {Dina A.} and Simmons, {Christine Q.} and Case, {Thomas C.} and Jia Yi and Cates, {Justin M.} and John Virostko and Xiusheng He and Xunbo Jin and Hayward, {Simon W.} and Matusik, {Robert J.} and AlfredL George and Yajun Yi",

note = "Funding Information: Grant Support: This work was supported in part by a Howard Temin Award from the National Cancer Institute at the National Institutes of Health ( CA114033 to YY), American Cancer Society-Institutional Research Grant (# IRG-58-009-51 and # IRG-58-009-53 ), and the Vanderbilt Clinical and Translational Science Awards (CTSA) UL1 RR024975 from National Center for Research Resources (NCRR) , a part of the National Institutes of Health (NIH) , ( CRC1838 to YY), and the National Cancer Institute ( 4R01-CA076142-14 to RJM ). DJD was supported by the American Cancer Society Great Lakes Division-Michigan Cancer Research Fund Postdoctoral Fellowship . The authors thank Dr. Harold L Moses and Dr. Jennifer Pietenpol for assistance in experiments; Dr. K. Pienta for providing bioluminescent human prostate carcinoma cell line (PC3-Luc); The Vanderbilt Cooperative Human Tissue Network for human tissue samples. Appendix A ",

year = "2013",

month = dec,

doi = "10.1016/j.molonc.2013.07.008",

language = "English (US)",

volume = "7",

pages = "1019--1030",

journal = "Molecular oncology",

issn = "1574-7891",

publisher = "Elsevier",

number = "6",

}

TY - JOUR

T1 - SPARCL1 suppresses metastasis in prostate cancer

AU - Xiang, Yuzhu

AU - Qiu, Qingchao

AU - Jiang, Ming

AU - Jin, Renjie

AU - Lehmann, Brian D.

AU - Strand, Douglas W.

AU - Jovanovic, Bojana

AU - DeGraff, David J.

AU - Zheng, Yi

AU - Yousif, Dina A.

AU - Simmons, Christine Q.

AU - Case, Thomas C.

AU - Yi, Jia

AU - Cates, Justin M.

AU - Virostko, John

AU - He, Xiusheng

AU - Jin, Xunbo

AU - Hayward, Simon W.

AU - Matusik, Robert J.

AU - George, AlfredL

AU - Yi, Yajun

N1 - Funding Information: Grant Support: This work was supported in part by a Howard Temin Award from the National Cancer Institute at the National Institutes of Health ( CA114033 to YY), American Cancer Society-Institutional Research Grant (# IRG-58-009-51 and # IRG-58-009-53 ), and the Vanderbilt Clinical and Translational Science Awards (CTSA) UL1 RR024975 from National Center for Research Resources (NCRR) , a part of the National Institutes of Health (NIH) , ( CRC1838 to YY), and the National Cancer Institute ( 4R01-CA076142-14 to RJM ). DJD was supported by the American Cancer Society Great Lakes Division-Michigan Cancer Research Fund Postdoctoral Fellowship . The authors thank Dr. Harold L Moses and Dr. Jennifer Pietenpol for assistance in experiments; Dr. K. Pienta for providing bioluminescent human prostate carcinoma cell line (PC3-Luc); The Vanderbilt Cooperative Human Tissue Network for human tissue samples. Appendix A

PY - 2013/12

Y1 - 2013/12

N2 - 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 invitro 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 invivo. Results: SPARCL1 expression did not inhibit tumor cell proliferation invitro. By contrast, SPARCL1 did suppress tumor cell migration and invasiveness invitro and tumor metastatic growth invivo, conferring improved survival in xenograft mouse models. Conclusions: We present the first invivo data suggesting that SPARCL1 suppresses metastasis of prostate cancer.

AB - 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 invitro 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 invivo. Results: SPARCL1 expression did not inhibit tumor cell proliferation invitro. By contrast, SPARCL1 did suppress tumor cell migration and invasiveness invitro and tumor metastatic growth invivo, conferring improved survival in xenograft mouse models. Conclusions: We present the first invivo data suggesting that SPARCL1 suppresses metastasis of prostate cancer.

KW - Gene expression signature

KW - Meta-analysis

KW - Metastasis

KW - Prostate cancer

KW - SPARCL1 function invivo

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DO - 10.1016/j.molonc.2013.07.008

M3 - Article

C2 - 23916135

AN - SCOPUS:84887995413

SN - 1574-7891

VL - 7

SP - 1019

EP - 1030

JO - Molecular oncology

JF - Molecular oncology

IS - 6

ER -

SPARCL1 suppresses metastasis in prostate cancer

Abstract

Keywords

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