Mechanism involving blm gene underlies repair of DNA damage of Jurkat cells induced by mitomycin C.
- Author:
Xue YI
1
;
Hui CHENG
;
Ping ZOU
;
Ling-Bo LIU
;
Ting ZHANG
;
Dan YU
;
Xiao-Ming ZHU
;
Liang ZOU
Author Information
1. Department of Hematology, Wuhan First Hospital, and Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Cycle;
DNA Damage;
drug effects;
DNA Repair;
drug effects;
Humans;
Jurkat Cells;
Mitomycin;
pharmacology;
RecQ Helicases;
genetics
- From:
Journal of Experimental Hematology
2010;18(5):1155-1158
- CountryChina
- Language:Chinese
-
Abstract:
The defect or block of apoptosis is an important factor involved in the drug resistance of tumor cells. Blm gene plays a great role in DNA damage and repair. This study was aimed to explore the relationship of blm gene expression with cell cycle and apoptosis after Jurkat DNA damage. The apoptosis rate and change of cell cycle were detected by flow cytometry, the expression level of blm mRNA in Jurkat cells was determined by semi-quantitative RT-PCR. The results indicated that after induction with 0.4 g/L of mitomycin C (MMC) for 24 hours the apoptosis rate of Jurkat cells were (11.42±0.013)%, and (66.08±1.60)% Jurkat cells were arrested in G2/M phase. After induction for 48 hours, the apoptosis rate of Jurkat cells declined from (11.42±0.013)% to (8.08±0.27)%, and cell count of Jurkat cells arrested in G2/M phase decreased from (66.08±1.60)% to (33.96±1.05)%. When induced with 0.4 g/L of MMC for 24 hours, the apoptosis rate of fibroblasts and the percentage of fibroblasts in G2/M, G0-G1 and S phase all showed no significant change until 48 hours. The range of apoptosis rate and the change of cell percentage in three phases were significantly different between Jurkat cells and fibroblasts (p<0.01). Expression level of blm mRNA in Jurkat cells was remarkably higher than that in normal fibroblasts (p<0.01), at 48 hours expression level of blm mRNA was remarkably higher than that at 24 hours. The 2 groups showed clear difference of blm mRNA expression after treated by MMC (p<0.01). It is concluded that the blm gene may play a significant role in repair of DNA damage of Jurkat cells after MMC induction. Abnormal expression of blm is correlated to the drug resistance of leukemia cells.
