Molecular Signatures of the Insulin-Like Growth Factor 1-Mediated Epithelial-Mesenchymal Transition in Breast, Lung and Gastric Cancers

• Main Authors: Armando Cevenini, Stefania Orrù, Annamaria Mancini, Andreina Alfieri, Pasqualina Buono, Esther Imperlini
• Format: Article
• Language: English
• Published: MDPI AG 2018-08-01
• Series: International Journal of Molecular Sciences
• Subjects: insulin-like growth factor 1 (IGF-1); IGF-1 receptor (IGF-1R); epithelial-mesenchymal transition (EMT); cancer; metastasis; PI3K/AKT pathway; RAS/MEK/ERK pathway
• Online Access: http://www.mdpi.com/1422-0067/19/8/2411

The insulin-like growth factor (IGF) system, which is constituted by the IGF-1 and IGF-2 peptide hormones, their corresponding receptors and several IGF binding proteins, is involved in physiological and pathophysiological processes. The IGF system promotes cancer proliferation/survival and its signaling induces the epithelial-mesenchymal transition (EMT) phenotype, which contributes to the migration, invasiveness, and metastasis of epithelial tumors. These cancers share two major IGF-1R signaling transduction pathways, PI3K/AKT and RAS/MEK/ERK. However, as far as we could review at this time, each type of cancer cell undergoes EMT through tumor-specific routes. Here, we review the tumor-specific molecular signatures of IGF-1-mediated EMT in breast, lung, and gastric cancers.