The mechanism of STAT5-ROS signal pathway to mediated imatinib resistance of K562 cells
10.19405/j.cnki.issn1000-1492.2017.07.008
- VernacularTitle:STAT5-ROS信号通路介导K562细胞伊马替尼耐药的机制研究
- Author:
Yingchan HAO
;
Xiucai XU
- Keywords:
chronic myeloid leukemia;
imatinib resistance;
STAT5-ROS signal pathway
- From:
Acta Universitatis Medicinalis Anhui
2017;52(7):979-983
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of STAT5-ROS pathway to mediate IM resistance of K562 cells.K562 cells were cultured with imatinib at gradually increased concentrations to generate resistance cell line.Methods CCK-8 assay was used to clarify the resistance ratio.The STAT5A and STAT5B mRNA levels were detected by RT-PCR.Flow cytometry assay was used to detect the level of ROS and cell apoptosis.The expression of STAT5 protein was detected by Western blot.Results Imatinib resistance cell line K562/G was successfully induced by gradually increasing concentrations of IM.The IC50 of K562/G was eighty times higher than K562 by CCK-8.Cell growth curve showed that K562/G was not inhibited in 20 μmol/L imatinib, whereas the K562 cell was significantly inhibited by up to 0.1 μmol/L imatinib.Intracellular level of ROS in K562/G was obviously higher than that of K562 cells(P=0.000 1).The apoptosis ratio of K562 was lower than that of K562/G when the same concentration of IM react on the two cell lines for the same time(P<0.05).The expression of STAT5A and STAT5B mRNA in K562/G was higher than in K562(P=0.000 1,P=0.017 0).Then,the level of STAT5 proteins in K562/G cells was significantly increased (P=0.009 0).Conclusion The STAT5 is highly expressed in CML.STAT5-ROS is closely related to the formation of imatinib resistance of chronic myeloid leukemia.
