AKT-induced PKM2 phosphorylation signals for IGF-1-stimulated cancer cell growth = AKT에의한 PKM2 인산화 시그널을 통한 IGF 유도 암세포 성장조절

Cited 39 time in scopus
Metadata Downloads
Title
AKT-induced PKM2 phosphorylation signals for IGF-1-stimulated cancer cell growth = AKT에의한 PKM2 인산화 시그널을 통한 IGF 유도 암세포 성장조절
Author(s)
Young Soo Park; Dong Joon Kim; Han Koo; S H Jang; Yeon Mi You; Jung Hee Cho; Suk-Jin Yang; E S Yu; Yuri Jung; Dong Chul LeeJung Ae Kim; Z Y Park; Kyung Chan Park; Young Il Yeom
Bibliographic Citation
Oncotarget, vol. 7, no. 30, pp. 48155-48167
Publication Year
2016
Abstract
Pyruvate kinase muscle type 2 (PKM2) exhibits post-translational modifications in response to various signals from the tumor microenvironment. Insulin-like growth factor 1 (IGF-1) is a crucial signal in the tumor microenvironment that promotes cell growth and survival in many human cancers. Herein, we report that AKT directly interacts with PKM2 and phosphorylates it at Ser-202, which is essential for the nuclear translocation of PKM2 protein under stimulation of IGF-1. In the nucleus, PKM2 binds to STAT5A and induces IGF-1-stimulated cyclin D1 expression, suggesting that PKM2 acts as an important factor inducing STAT5A activation under IGF-1 signaling. Concordantly, overexpression of STAT5A in cells deficient in PKM2 expression failed to restore IGF-induced growth, whereas reconstitution of PKM2 in PKM2 knockdown cells restored the IGF-induced growth capacity. Our findings suggest a novel role of PKM2 in promoting the growth of cancers with dysregulated IGF/phosphoinositide 3-kinase/AKT signaling.
Keyword
AKTIGF-1Phosphorylation of PKM2PKM2STAT5
ISSN
1949-2553
Publisher
Impact Journals
DOI
http://dx.doi.org/10.18632/oncotarget.10179
Type
Article
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Aging Convergence Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.