Insulin signal transduction in normal cells and its role in carcinogenesis.
Convincing epidemiological evidence exists for a causal relationship between increased risk of cancer development and progression and type 2 diabetes mellitus as well as obesity. Though the underlying mechanisms remain elusive, in light of the well-described mitogenic actions of insulin, hyperinsulinaemia in the presence of insulin resistance is probably a key factor. In this short review, an overview over the insulin signalling cascade is given paying special attention to the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI 3-K)/mammalian target of rapamycin (mTOR) pathways which are involved in protein synthesis and cell growth.
Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, Department of Internal Medicine, University Hospital of Tübingen, Tübingen, Germany.
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Müssig
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Häring
D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications*; D006801:Humans; D006946:Hyperinsulinism; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance / Q000502:physiology; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009369:Neoplasms / Q000453:epidemiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D012016:Reference Values; D015398:Signal Transduction / Q000502:physiology*; D058570:TOR Serine-Threonine Kinases
D007328:Insulin; D047908:Intracellular Signaling Peptides and Proteins; D020928:Mitogen-Activated Protein Kinases; D019869:Phosphatidylinositol 3-Kinases; D017346:Protein Serine-Threonine Kinases; D058570:TOR Serine-Threonine Kinases; C546842:MTOR protein, human