Inhibition of decay-accelerating factor (CD55) attenuates prostate cancer growth and survival in vivo

Robert D. Loberg; La Shon L. Day; Rodney Dunn; Linda M. Kalikin; Kenneth J. Pienta

doi:10.1593/neo.05679

Inhibition of decay-accelerating factor (CD55) attenuates prostate cancer growth and survival in vivo

Robert D. Loberg, La Shon L. Day, Rodney Dunn, Linda M. Kalikin, Kenneth J. Pienta

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

53 Scopus citations

Abstract

Decay-accelerating factor (CD55) is a member of membrane-bound complement-regulatory proteins. CD55 expression correlates with poor survival in patients with colorectal cancer and has been implicated in the survival and tumorigenesis of blood-borne malignancies. Histologic analysis of clinical specimens from patients with advanced prostate cancer revealed an increase in CD55 expression in prostate tumor epithelial cells. CD55 was shown to be functionally active and to inhibit complement-mediated lysis in PC-3 and DU145 cells. The percentage of lysis was correlative with the CD55 expression profile observed in these prostate cancer cell lines. These data suggest that CD55 is an important regulator of prostate cancer cell survival. As a result, we have hypothesized that CD55 expression on prostate cancer cells promotes cell survival and contributes to the metastatic potential of prostate cancer cells. To determine the role of CD55 in prostate cancer tumorigenesis and metastasis, we generated PC-3^Luc prostate cancer cells with CD55 siRNA-targeted disruption. We found that PC-3^Luc/CD55 siRNA constructs in SCID mice resulted in a significant attenuation of overall tumor burden. Further investigation into the mechanisms of CD55-mediated tumor cell/microenvironment interaction is necessary to understand the role of CD55 in tumor cell survival and metastatic lesion formation.

Original language	English (US)
Pages (from-to)	69-78
Number of pages	10
Journal	Neoplasia
Volume	8
Issue number	1
DOIs	https://doi.org/10.1593/neo.05679
State	Published - Jan 2006
Externally published	Yes

Keywords

CD55
Cancer
Complement
DAF
Prostate

ASJC Scopus subject areas

Cancer Research

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10.1593/neo.05679

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title = "Inhibition of decay-accelerating factor (CD55) attenuates prostate cancer growth and survival in vivo",

abstract = "Decay-accelerating factor (CD55) is a member of membrane-bound complement-regulatory proteins. CD55 expression correlates with poor survival in patients with colorectal cancer and has been implicated in the survival and tumorigenesis of blood-borne malignancies. Histologic analysis of clinical specimens from patients with advanced prostate cancer revealed an increase in CD55 expression in prostate tumor epithelial cells. CD55 was shown to be functionally active and to inhibit complement-mediated lysis in PC-3 and DU145 cells. The percentage of lysis was correlative with the CD55 expression profile observed in these prostate cancer cell lines. These data suggest that CD55 is an important regulator of prostate cancer cell survival. As a result, we have hypothesized that CD55 expression on prostate cancer cells promotes cell survival and contributes to the metastatic potential of prostate cancer cells. To determine the role of CD55 in prostate cancer tumorigenesis and metastasis, we generated PC-3Luc prostate cancer cells with CD55 siRNA-targeted disruption. We found that PC-3Luc/CD55 siRNA constructs in SCID mice resulted in a significant attenuation of overall tumor burden. Further investigation into the mechanisms of CD55-mediated tumor cell/microenvironment interaction is necessary to understand the role of CD55 in tumor cell survival and metastatic lesion formation.",

keywords = "CD55, Cancer, Complement, DAF, Prostate",

author = "Loberg, {Robert D.} and Day, {La Shon L.} and Rodney Dunn and Kalikin, {Linda M.} and Pienta, {Kenneth J.}",

note = "Funding Information: Address all correspondence to: Robert D. Loberg, PhD, University of Michigan Urology Center, 7431 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0946. E-mail: [email protected] 1This work was supported, in part, by National Cancer Institute grants (SPORE) PO1 and RO1. We would like to thank the AFUD Scholarship Program for supporting R.D.L. as an AFUD scholar. Received 10 October 2005; Revised 4 November 2005; Accepted 7 November 2005.",

year = "2006",

month = jan,

doi = "10.1593/neo.05679",

language = "English (US)",

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AU - Loberg, Robert D.

AU - Day, La Shon L.

AU - Dunn, Rodney

AU - Kalikin, Linda M.

AU - Pienta, Kenneth J.

N1 - Funding Information: Address all correspondence to: Robert D. Loberg, PhD, University of Michigan Urology Center, 7431 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0946. E-mail: [email protected] 1This work was supported, in part, by National Cancer Institute grants (SPORE) PO1 and RO1. We would like to thank the AFUD Scholarship Program for supporting R.D.L. as an AFUD scholar. Received 10 October 2005; Revised 4 November 2005; Accepted 7 November 2005.

PY - 2006/1

Y1 - 2006/1

N2 - Decay-accelerating factor (CD55) is a member of membrane-bound complement-regulatory proteins. CD55 expression correlates with poor survival in patients with colorectal cancer and has been implicated in the survival and tumorigenesis of blood-borne malignancies. Histologic analysis of clinical specimens from patients with advanced prostate cancer revealed an increase in CD55 expression in prostate tumor epithelial cells. CD55 was shown to be functionally active and to inhibit complement-mediated lysis in PC-3 and DU145 cells. The percentage of lysis was correlative with the CD55 expression profile observed in these prostate cancer cell lines. These data suggest that CD55 is an important regulator of prostate cancer cell survival. As a result, we have hypothesized that CD55 expression on prostate cancer cells promotes cell survival and contributes to the metastatic potential of prostate cancer cells. To determine the role of CD55 in prostate cancer tumorigenesis and metastasis, we generated PC-3Luc prostate cancer cells with CD55 siRNA-targeted disruption. We found that PC-3Luc/CD55 siRNA constructs in SCID mice resulted in a significant attenuation of overall tumor burden. Further investigation into the mechanisms of CD55-mediated tumor cell/microenvironment interaction is necessary to understand the role of CD55 in tumor cell survival and metastatic lesion formation.

AB - Decay-accelerating factor (CD55) is a member of membrane-bound complement-regulatory proteins. CD55 expression correlates with poor survival in patients with colorectal cancer and has been implicated in the survival and tumorigenesis of blood-borne malignancies. Histologic analysis of clinical specimens from patients with advanced prostate cancer revealed an increase in CD55 expression in prostate tumor epithelial cells. CD55 was shown to be functionally active and to inhibit complement-mediated lysis in PC-3 and DU145 cells. The percentage of lysis was correlative with the CD55 expression profile observed in these prostate cancer cell lines. These data suggest that CD55 is an important regulator of prostate cancer cell survival. As a result, we have hypothesized that CD55 expression on prostate cancer cells promotes cell survival and contributes to the metastatic potential of prostate cancer cells. To determine the role of CD55 in prostate cancer tumorigenesis and metastasis, we generated PC-3Luc prostate cancer cells with CD55 siRNA-targeted disruption. We found that PC-3Luc/CD55 siRNA constructs in SCID mice resulted in a significant attenuation of overall tumor burden. Further investigation into the mechanisms of CD55-mediated tumor cell/microenvironment interaction is necessary to understand the role of CD55 in tumor cell survival and metastatic lesion formation.

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KW - Complement

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Inhibition of decay-accelerating factor (CD55) attenuates prostate cancer growth and survival in vivo

Abstract

Keywords

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