AACR Meeting Abstracts
HOME HELP FEEDBACK HOW TO CITE ABSTRACTS ARCHIVE CME INFORMATION SEARCH
Cancer ResearchClinical Cancer Research
Cancer Epidemiology Biomarkers & PreventionMolecular Cancer Therapeutics
Molecular Cancer ResearchCancer Prevention Research
Cancer Prevention Journals PortalCancer Reviews Online
Annual Meeting Education BookMeeting Abstracts Online
 QUICK SEARCH:   [advanced]




This Article
Services
Right arrow Similar articles in this journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Singh, S.
Right arrow Articles by Lillard, J. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Singh, S.
Right arrow Articles by Lillard, J. W., Jr
[Proc Amer Assoc Cancer Res, Volume 45, 2004]


Cellular, Molecular, and Tumor Biology 33: Inflammation and Metastasis

Abstract #1763

CXCR5-mediated prostate cancer cell migration and invasion

Shailesh Singh, Udai P. Singh, William E. Grizzle and James W. Lillard, Jr

Morehouse School of Medicine, Atlanta, GA and University of Alabama at Birmingham, Birmingham, AL

Chemokine-chemokine receptor interactions can induce chemotaxis and invasion. Indeed, other studies have demonstrated that the functional expression of CXCR4 by prostate cancer cells can enhance cancer cell metastasis. Here we show that CXCR5 is functionally expressed by prostate cancer cells. Interestingly, LNCaP, which is potentially less metastatic than PC3 cells in vivo, expresses higher levels of CXCR5 mRNA than PC3. Both LNCaP and PC3 cell lines expressed higher levels of CXCR5 than normal prostatic epithelial cells (PrEC). We also investigated the influence of CXCL13-CXCR5 ligation on migration and invasion. After CXCL13-engagement, LNCaP cells displayed a higher migration and invasive potential in vitro than PC3 cells, which was significantly reduced by CXCR5 blockade. The CXCL13-mediated enhanced invasive capacity was most likely the result of matrix metalloproteinase (MMPs) modulation. In this regard, CXCL13 increased collagenase-1 (MMP-1), collagenase-3 (MMP-13), stromalysin-1 (MMP-3), stromalysin-2 (MMP-10), and stromalysin-3 (MMP-11) expression by both LNCaP and PC3 cell lines. These data suggest that the expression and ligation of CXCR5 with CXCL13 by prostate cancer cells affects migration, invasion and MMP expression of prostate cancer cells.







HOME HELP FEEDBACK HOW TO CITE ABSTRACTS ARCHIVE CME INFORMATION SEARCH
Cancer ResearchClinical Cancer Research
Cancer Epidemiology Biomarkers & PreventionMolecular Cancer Therapeutics
Molecular Cancer ResearchCancer Prevention Research
Cancer Prevention Journals PortalCancer Reviews Online
Annual Meeting Education BookMeeting Abstracts Online
Copyright © 2004 by the American Association for Cancer Research.