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Plasminogen activator inhibitor 1 - insulin-like growth factor binding protein 3 cascade regulates stress-induced senescence
Author(s) -
David J. Elzi,
Yanlai Lai,
Meihua Song,
Kevin Hakala,
Susan T. Weintraub,
Yuzuru Shiio
Publication year - 2012
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1120437109
Subject(s) - senescence , activator (genetics) , mediator , microbiology and biotechnology , plasminogen activator , growth factor , biology , igfbp3 , proteolysis , plasminogen activator inhibitor 1 , insulin like growth factor binding protein , extracellular , insulin like growth factor , biochemistry , receptor , endocrinology , enzyme
Cellular senescence is widely believed to play a key role in tumor suppression, but the molecular pathways that regulate senescence are only incompletely understood. By using a secretome proteomics approach, we identified insulin-like growth factor binding protein 3 (IGFBP3) as a secreted mediator of breast cancer senescence upon chemotherapeutic drug treatment. The senescence-inducing activity of IGFBP3 is inhibited by tissue-type plasminogen activator-mediated proteolysis, which is counteracted by plasminogen activator inhibitor 1 (PAI-1), another secreted mediator of senescence. We demonstrate that IGFBP3 is a critical downstream target of PAI-1-induced senescence. These results suggest a role for an extracellular cascade of secreted proteins in the regulation of cellular senescence.

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