Advancement of insulin effecting signaling pathway of leukemia cell proliferation.
- Author:
Yue-Qin HUANG
1
;
Jing-Xin PAN
Author Information
1. Department of Hematology, Fujian Medical University, Quanzhou, Fujian Province, China.
- Publication Type:Journal Article
- MeSH:
Cell Line, Tumor;
Cell Proliferation;
Humans;
Insulin;
Insulin-Like Growth Factor I;
metabolism;
Leukemia;
metabolism;
pathology;
Receptor, Insulin;
metabolism;
Signal Transduction
- From:
Journal of Experimental Hematology
2012;20(2):514-517
- CountryChina
- Language:Chinese
-
Abstract:
Many reports have documented a role of insulin and insulin-like growth factor 1 (IGF-1) as growth factors in many cancers. The sequence and structure of insulin receptor (IR) and IGF receptor (IGF-1R) are highly similar. Both receptors are overexpressed in leukemia cells.Studies indicate that insulin can enhance the signal of the phosphoinositide 3-kinase/Akt pathways by activating IR or IGF-1R or hybrid IR/IGF-IR receptors, resulting in the proliferation of leukemia cells. High concentration of insulin may inhibit the growth of leukemia cells, the mechanism of which remains to be unclear. Inhibiting IR and IGF-IR can diminish the proliferation of leukemia cells. Therefore, the assumption of IR/IGF-1R as a potential therapeutic target in leukemia appears reasonable. This article summarizes the recent advancement associated with the signaling pathway of insulin effecting the proliferation of leukemia cells.
