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G proteins associated with CXCR5 expressed by prostate cancer cells
Author(s) -
El Haibi Christelle P,
Singh Shailesh,
Sharma Praveen K.,
Lillard James W.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.666.12
Subject(s) - prostate cancer , cancer research , cxcr5 , cxcl13 , ccl21 , bone metastasis , chemokine , biology , chemokine receptor , receptor , cancer , medicine , biochemistry
Metastasis to bone remains a major clinical concern and the main cause of prostate cancer (PCa) morbidity and mortality. The reasons for preferential establishment and growth of disseminated PCa cells in bone marrow are incompletely understood and require further investigation. We have recently shown that PCa cell lines differentially express CXCR5, and in vivo CXCR5 expression positively correlates with prostate tumor staging, as determined by histological staining of surgical specimens and tissue microarrays. By virtue of its presence in the bone microenvironment, CXCL13 (the ligand for CXCR5) may play a critical role in PCa cell migration and invasion, when compared to normal prostatic epithelial cells. Like other chemokine receptors, CXCR5 is a cell surface G‐protein coupled receptor. We have delineated some events triggered by G‐protein activation through CXCL13 binding to CXCR5 expressed by PCa cell lines derived from bone, brain, and lymph node metastases. G‐protein isoforms expressed by these PCa cell lines were evaluated by Western Blot, while tandem mass spectrometry analysis was used to elucidate the proteins that associate with CXCR5 before and after CXCL13 interaction. We show that PCa cells differentially express G‐protein isoforms to presumably modulate PCa progression in part through CXCR5 activation. This research is supported by USAMRMC (Award # W81XWH‐06‐01‐9562).