Insulin Receptor Substrate Regulation of Phosphoinositide 3-Kinase

Insulin receptor substrates (IRS) serve as downstream messengers from activated cell surface receptors to numerous signaling pathway cascades. One of these pathways, phosphoinositide 3-kinase (PI3K), frequently displays aberrant function in the setting of cancer. IRS proteins are capable of both reg...

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Bibliographic Details
Published in:Clinical cancer research 2011-01, Vol.17 (2), p.206-211
Main Authors: METZ, Heather E, MCGARRY HOUGHTON, A
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 4-Kinase - metabolism
Antineoplastic agents
Biological and medical sciences
Gene Expression Regulation
Humans
Insulin Receptor Substrate Proteins - physiology
Leukocyte Elastase - metabolism
Medical sciences
Neoplasms - metabolism
Pharmacology. Drug treatments
Signal Transduction
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Summary:Insulin receptor substrates (IRS) serve as downstream messengers from activated cell surface receptors to numerous signaling pathway cascades. One of these pathways, phosphoinositide 3-kinase (PI3K), frequently displays aberrant function in the setting of cancer. IRS proteins are capable of both regulating and activating PI3K, depending on the cell of origin. As such, both prohost and protumor functions have been described for IRS proteins in human cancers. IRS proteins may eventually serve as biomarkers of PI3K activity, and serve a much-needed role as a guide to using targeted pathway therapy. Additionally, IRS-1 could be indirectly targeted in lung cancer, by inhibiting neutrophil elastase, which functions to degrade IRS-1 in lung tumor cells, thereby generating PI3K hyperactivity.
ISSN:1078-0432
1557-3265
DOI:10.1158/1078-0432.ccr-10-0434