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Signalling pathways involved in antiproliferative effects of IGFBP-3: a review Baxter RCMol Pathol 2001[Jun]; 54 (3): 145-8Insulin-like growth factor binding protein-3 (IGFBP-3), the major circulating carrier protein for IGFs, is also active in the cellular environment as a potent antiproliferative agent. It appears to function both by cell cycle blockade and the induction of apoptosis. Transfection of p53 negative T47D breast cancer cells to express IGFBP-3 leads to induction of the apoptotic protein bax and an increase in sensitivity to ionising radiation. IGFBP-3 can be transported to the nucleus by an importin beta mediated mechanism, where it has been shown to interact with the retinoid X receptor alpha and possibly other nuclear elements. Expression of oncogenic ras is associated with resistance to exogenous IGFBP-3, the effect being reversible by inhibition of mitogen activated protein (MAP) kinase phosphorylation. IGFBP-3 antiproliferative signalling appears to require an active transforming growth factor beta (TGF-beta) signalling pathway, and IGFBP-3 stimulates phosphorylation of the TGF-beta signalling intermediates Smad2 and Smad3. These recent findings all point to a complex intracellular mode of action of IGFBP-3, which will need to be better understood if anti-cancer treatments are to take advantage of the antiproliferative activity of IGFBP-3.|Apoptosis/physiology[MESH]|Cell Cycle/physiology[MESH]|Cell Division/physiology[MESH]|Humans[MESH]|Insulin-Like Growth Factor Binding Protein 3/*physiology[MESH]|Mitogen-Activated Protein Kinases/physiology[MESH]|Phosphorylation[MESH]|Proto-Oncogene Proteins p21(ras)/physiology[MESH]|Signal Transduction/*physiology[MESH]|Transforming Growth Factor beta/physiology[MESH]|Tumor Cells, Cultured/physiology[MESH] |
