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4106708 
Journal Article 
Insulin-like growth factor 1 promotes growth of gastric cancer by inhibiting foxo1 nuclear retention 
Li, S; Lei, X; Zhang, J; Yang, H; Liu, J; Xu, C 
2015 
1 
Tumor Biology
ISSN: 1010-4283
EISSN: 1423-0380 
36 
6 
4519-4523 
English 
25596089 
WOS:000359383700059 
has retraction 4098513 Retraction Note to multiple articles in Tumor Biology
Gastric cancer (GC) is the fourth most common malignant human cancer. So far, the molecular mechanisms underlying the tumorigenesis of GC are not completely understood. Here, we reported significantly higher levels of serum insulin-like growth factor (IGF)-1 in GC patients and significantly higher levels of phosphorylated IGF-1 receptor (IGF-1R) in the GC specimen. Moreover, IGF-1 induced phosphorylation of IGF-1R and then phosphorylation of its downstream factor Akt in the GC cells. Further, IGF-1/Akt-induced forkhead box protein O1 (FoxO1) nuclear exclusion, but not IGF-1/Akt-induced mTOR phosphorylation, was essential for the augment in GC cell growth. Together, IGF-1/Akt/FoxO1 regulatory machinery appears to be a previously unappreciated signaling axis involved in the carcinogenesis of GC.