Insulin In Cancer Research Articles

Disrupting Insulin-Like Growth Factor Signaling as a Potential Cancer Therapy

The type I insulin-like growth factor receptor (IGF-IR) plays multiple roles in several cancers and increased circulating levels of insulin-like growth factor-I (IGF-I) are associated with increased risk of breast, colon, and prostate cancers. Because IGF-II and insulin signal via the insulin receptor (IR) to stimulate the growth of cancer cells, inhibition of IR might be necessary to totally disrupt the action of IGFs and their receptors. This review describes the well-recognized roles of IGF-IR in driving the malignant phenotype, examines the evidence that perhaps IR should also be targeted to inhibit the effects of the IGF ligands and insulin in cancer, describes the strategies to disrupt IGF signaling in cancer, and highlights some key issues that need to be considered as clinical trials targeting IGF-IR proceed.

Disrupting insulin-like growth factor signaling as a potential cancer therapy

The type I insulin-like growth factor receptor (IGF-IR) plays multiple roles in several cancers and increased circulating levels of insulin-like growth factor-I (IGF-I) are associated with increased risk of breast, colon, and prostate cancers. Because IGF-II and insulin signal via the insulin receptor (IR) to stimulate the growth of cancer cells, inhibition of IR might be necessary to totally disrupt the action of IGFs and their receptors. This review describes the well-recognized roles of IGF-IR in driving the malignant phenotype, examines the evidence that perhaps IR should also be targeted to inhibit the effects of the IGF ligands and insulin in cancer, describes the strategies to disrupt IGF signaling in cancer, and highlights some key issues that need to be considered as clinical trials targeting IGF-IR proceed.

Insulin and cancer (Review)

Although the molecular mechanisms of insulin action on many physiological and biochemical processes are far from being completely understood, little doubt exists about the involvement of insulin in tumoural processes. Indeed, increased insulin production (either directly by the tumour in an ectopic fashion, or indirectly by stimulation of the pancreatic secretion) is a common phenomenon during cancer development. Paradoxically, the increased production and circulating levels of the hormone are associated with a decrease in sensitivity which leads to insulin resistance in the non-tumoural tissues, resulting in hyperlipaemia and profound alterations in carbohydrate and lipid metabolism. In addition to these effects on the host, insulin can actually increase the incidence of neoplasias and promote tumour growth. This is probably related to the signaling pathway of the hormone, which shares many elements with that of several growth factors. In addition, insulin signaling directly interacts with that of the ras oncogene. We review the involvement of insulin in cancer from a multidisciplinary point of view, with the aim of encouraging the design of future therapeutic options for cancer treatment.