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. 2003 Feb 18;88(4):606–612. doi: 10.1038/sj.bjc.6600739

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Copyright © 2003 Cancer Research UK

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Model for the inhibition of bradykinin-induced cPKCs translocation by gelsolin in PC10 cells. Tumour promotion mostly depended on the PKC signal transduction pathway via the route that activated PLCβ stimulated through a G-protein-coupled receptor. Gelsolin sequesters PIP2 and suppresses production of DAG and IP3 by PLCβ, and thereby translocation to membrane fraction and activation of cPKCs is inhibited. As the PLCβ/cPKCs pathway is critical for growth of lung cancer cells, and overexpression of gelsolin in PC10 cells results in the loss of tumorigenicty.