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 journalArticle

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.

Original languageEnglish (US)
Pages (from-to)69-78
Number of pages10
JournalNeoplasia
Volume8
Issue number1
DOIs
StatePublished - Jan 2006

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Keywords

  • CD55
  • Cancer
  • Complement
  • DAF
  • Prostate

ASJC Scopus subject areas

  • Cancer Research

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