Novel mechanism of IGF-binding protein-3 action on prostate cancer cells: Inhibition of proliferation, adhesion, and motility.
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19 avril 2011
- handle: 10670/1.abp6x6
- doi: 10.1677/ERC-08-0175
info:eu-repo/semantics/openAccess
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Biological SciencesSujets proches
Prostate gland Glandula prostata Prostata Gland, ProstateCiter ce document
Andrea Matscheski et al., « Novel mechanism of IGF-binding protein-3 action on prostate cancer cells: Inhibition of proliferation, adhesion, and motility. », Elektronisches Publikationsportal der Österreichischen Akademie der Wissenschafte, ID : 10.1677/ERC-08-0175
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Résumé
IGF-binding protein-3 (IGFBP-3) is a modulator of the IGF-signaling pathway and was described as an anti-cancer agent in prostate cancer. The molecular mechanisms underlying these effects remained, however, largely undefined. We analyzed the influence of recombinant IGFBP-3 on cell proliferation of PC3, Du145, and LNCaP prostate cancer cells. As expected, IGFBP-3 inhibited IGF-stimulated cell proliferation by blocking IGF-mediated proliferation signals, but we observed an IGF-independent inhibitory effect of IGFBP-3 on prostate cancer cell proliferation in long-term cultures. We further investigated the influence of IGFBP-3 on adhesion, motility, and invasion of prostate cancer cells using adhesion assays, live-cell imaging techniques, and matrigel invasion measurements. There was a clear inhibitory effect of IGFBP-3 on tumor cell adhesion to extracellular matrix components in the presence and absence of IGF, whereas cell–cell adhesion was not affected. The same inhibitory effect of IGFBP-3 was determined on cell motility when real-time cell movements were followed. In addition, IGFBP-3 was able to inhibit tumor cell invasion through matrigel. In summary, we show that IGFBP-3 inhibits proliferation, adhesion, migration, and invasion processes of prostate tumor cells. These newly described mechanisms of IGFBP-3 can be of importance for tumor progression and support a role of IGFBP-3 in therapeutic settings.