Abstract
The nuclear translocation of insulin-like growth factor receptor type 1 (IGF-1R) has been documented in a variety of previous studies. The exact mechanism of this translocation, however, is still poorly understood. Furthermore, the functional role of IGF-1R in the nucleus shows promise of transcriptional control. This function is particularly important in cancer cells. Understanding this role may also give insights into cancer biology and treatment methods. Processes including SUMOylation and clathrin-mediated endocytosis are necessary for IGF-1R nuclear translocation to occur. The antiapoptotic qualities of IGF-1R likely contribute to its function in cancer cells. This review aims to synthesize the work on IGF-1R in order to propose a mechanism of translocation. Using this mechanism, new therapeutic targets can be proposed that hinder the role of IGF-1R in cancer metastasis.
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