Effect of MAPK signaling pathway phosphorylation on proliferation of myeloma cell line KM3 by insulin-like growth factor 1.
- Author:
Hua-Fang WANG
1
;
Yu HU
;
Chun-Yan SUN
;
Ya-Dan WANG
Author Information
1. Institute of Hematology, Union Hospital, Tongji Medical college, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Cell Cycle;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Humans;
Insulin-Like Growth Factor I;
pharmacology;
MAP Kinase Signaling System;
physiology;
Mitogen-Activated Protein Kinase Kinases;
metabolism;
physiology;
Multiple Myeloma;
pathology;
Phosphorylation
- From:
Journal of Experimental Hematology
2007;15(5):978-981
- CountryChina
- Language:Chinese
-
Abstract:
In order to study the effect of insulin-like growth factor 1 (IGF-1) on proliferation of myeloma cell line KM3 and the role of MAPK pathway phosphorylation in this process, the cell cycle distribution shift of KM3 after incubation with series concentration of IGF-1 was detected by flow cytometry. Phosphorate-Erk1/2, the key molecule of MAPK pathway, was examined by Western blot after KM3 cells being pretreated with or without PD98059, the special inhibitor of Erk1 and Erk2 phosphorylation. The effect of specifically blocking Erk1 and Erk2 phosphorylation on proliferation and apoptosis of KM3 cells were detected with TUNEL staining. The results showed that the KM3 cells at S and G2/M phase increased and the phosphorylation of Erk1 and Erk2 became intensive when incubated with different concentration of IGF-1. PD98059 could decrease the phosphorylation of Erk1/2 induced by IGF-1 and induce the apoptosis of KM3 cells. It is concluded The phosphorylation of MAPK signaling pathway triggered by IGF-1 plays an important role in the proliferation of myeloma cell line KM3.
