Record number :
Title of article :
GIPC mediates the generation of reactive oxygen species and the regulation of cancer cell proliferation by insulin-like growth factor-1/IGF-1R signaling
Author/Authors :
Choi، نويسنده , , Ji Seung and Paek، نويسنده , , A Rome and Kim، نويسنده , , Soo Youl and You، نويسنده , , Hye Jin، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2010
Pages :
From page :
To page :
Abstract :
Insulin-like growth factor-1 (IGF-1)/IGF-1 receptor signaling participates in a variety of cellular processes, including cell survival, growth, and proliferation. Increased expression of IGF-1R and activation of its downstream signaling components have been implicated in human cancers. Although a regulatory role for IGF-1R has been established, the relationship between IGF-1R and its binding partner, GAIP-interacting protein C-terminus (GIPC), in terms of promoting cell proliferation, remains unclear. We found that siRNA-mediated silencing of GIPC expression decreased IGF-1-mediated IGF-1R phosphorylation and cellular proliferation in breast cancer models. IGF-1-mediated cellular proliferation was also inhibited by N-acetylcysteine, which implicates reactive oxygen species generation. siRNA-mediated silencing of GIPC expression also decreased IGF-1-mediated reactive oxygen species generation. Taken together, these data suggest that GIPC contributes to IGF-1-induced cancer cell proliferation via the regulation of reactive oxygen species production.
Keywords :
IGF-1 signaling , GIPC , PI3-kinase/Akt , Reactive oxygen species , growth regulation
Journal title :
Cancer Letters
Journal title :
Cancer Letters
Serial Year :
Link To Document :