Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 269, Issue 3, Pages 652-659Publisher
ACADEMIC PRESS INC
DOI: 10.1006/bbrc.2000.2343
Keywords
Rho-kinase; prostate cancer; metastasis; cell migration; Y-27632; angiogenesis; myosin phosphatase
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Funding
- NCI NIH HHS [P30CA44579] Funding Source: Medline
- NHLBI NIH HHS [P01HL19242, P01HL48807] Funding Source: Medline
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The Rho-kinase inhibitor, Y-27632, inhibited in vitro chemotactic migration to bone marrow fibroblast conditioned media and metastatic growth in immune-compromised mice of highly invasive human prostatic cancer (PC3) cells. Y-27632 also reduced myosin light chain phosphorylation and markedly altered the morphology of cells that developed numerous processes containing microtubules. A strikingly different, rounded phenotype was induced by an inhibitor of myosin light chain kinase, ML9. The M110-130 subunit of the myosin phosphatase that is regulated by Rho-kinase was present in PC3 cells that contained significantly more RhoA than the less invasive, LNCaP cells. Y-27632 also inhibited angiogenesis as measured by endothelial cell tube formation on Matrigel. We conclude that invasiveness of human prostate cancer is facilitated by the Rho/Rho-kinase pathway, and exploration of selective Rho-kinase inhibitors for limiting invasive progress of prostate cancer is warranted. (C) 2000 Academic Press.
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