Regulative effects of ERK and P38 signal transduction pathway on cell cycle in chronic myeloid leukemia.
- Author:
Xiao GUO
1
;
Ling PAN
;
Lan-Fen HOU
;
You-Jun WANG
;
Hon-Mou GUO
;
Lin YANG
;
Zhi-Wei WANG
;
Yu SUN
;
Dong-Liang LI
Author Information
1. Department of Hematology, Norman Bethune Interenational Peace Hospital, Shijiazhuang 050082, China.
- Publication Type:Journal Article
- MeSH:
Adult;
Cell Cycle;
physiology;
Cells, Cultured;
Extracellular Signal-Regulated MAP Kinases;
metabolism;
Female;
Humans;
K562 Cells;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
metabolism;
pathology;
Male;
Middle Aged;
Signal Transduction;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Journal of Experimental Hematology
2007;15(2):242-247
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the regulative effect of ERK and p38 signal transduction pathway on cell cycle of CML. The mRNA and protein expression of ERK, p38, cyclin D(2), cyclin E and p27 (ERK and p38 were Phosph-ERK and Phosph-P38) in CML cells and K562 cell lines were detected by RT-PCR and Western blot, respectively; cell cycle was determined by FCM, and their relationship was analyzed. The results showed that the mRNA and protein expressions of ERK, p38, cyclin D(2) and cyclin E in CML cells and K562 cells increased (P<0.01) and the expression of p27 decreased (P<0.01). There was positive correlation between the protein expressions of cyclin D(2) and the protein expression of ERK, p38 and cyclin E, but there was negative correlation between the protein expressions of cyclin D(2) and the protein expression of p27. The percentage of cells in G(0)/G(1) phase was decreased and the percentage of cells in S phase was increased, there was significant difference as compared with control (P<0.05). It is concluded that increase of the mRNA expression and protein activity of ERK and p38 activate the cell cycle-regulating proteins such as cyclin D(2), cyclin E, p27 which results in shortening of G(0)/G(1) phase, switching cell to S phase through G(1)/S check point quickly and accelerating cell cycle progression and cell proliferation, and eventually leads to occurrence of CML.
