The roles of PIKE in tumorigenesis

• Type of Material: Article
• Authors: Qi Qi, Emory University; Keqiang Ye, Emory University
• Language: English
• Date: 2013-08-05
• Publisher: Nature Publishing Group: Open Access Hybrid Model Option A
• Publication Version: Final Published Version
• Copyright Statement: © 2013 CPS and SIMM
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://www.nature.com/aps/journal/v34/n8/full/aps201371a.html
• Title of Journal or Parent Work: Acta Pharmacologica Sinica
• ISSN: 1671-4083
• Volume: 34
• Issue: 8
• Start Page: 991
• End Page: 997
• Grant/Funding Information: This work is supported by the National Institutes of Health grant No RO1 CA127119, USA (Keqiang YE).
• Keywords: phosphoinositide; PIKE; tumorigenesis; 3-kinase; cancer; Akt
• Research Categories: Health Sciences, Oncology; Health Sciences, Pathology; Health Sciences, Pharmacology

Abstract

Tumorigenesis is the process by which normal cells evolve the capacity to evade and overcome the constraints usually placed upon their growth and survival. To ensure the integrity of organs and tissues, the balance of cell proliferation and cell death is tightly maintained. The proteins controlling this balance are either considered oncogenes, which promote tumorigenesis, or tumor suppressors, which prevent tumorigenesis. Phosphoinositide 3-kinase enhancer (PIKE) is a family of GTP-binding proteins that possess anti-apoptotic functions and play an important role in the central nervous system. Notably, accumulating evidence suggests that PIKE is a proto-oncogene involved in tumor progression. The PIKE gene (CENTG1) is amplified in a variety of human cancers, leading to the resistance against apoptosis and the enhancement of invasion. In this review, we will summarize the functions of PIKE proteins in tumorigenesis and discuss their potential implications in cancer therapy.