Skip to main content
Fig. 5 | Experimental Hematology & Oncology

Fig. 5

From: The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

Fig. 5

KW-2478 inhibited the chaperone function of HSP90α and then weakened the BCR/ABL and MAPK signalling pathways. a The expression levels of BCR/ABL, p-BCR/ABL, STAT5 and p-STAT5 in CML cells after KW-2478 treatment were detected by western blots. b The expression levels of HSP90α, HSP90β, Grp94 and Hsp70 in CML cells after KW-2478 treatment were quantitatively analysed by western blot. c The mRNA level of BCR/ABL was detected with qRT-PCR. β-Actin was used as an internal control. d The mRNA level of HSP90α was detected with qRT-PCR. e The interaction between HSP90α and BCR/ABL was analysed by Co-IP assays with no KW-2478 treatment. f The influence of KW-2478 on the interaction between HSP90α and BCR/ABL was analysed by Co-IP assays. g Molecules in the MAPK signalling pathway, such as Ras, phospho-Raf1, Mek1/2, phosphorylated and total Erk1/2, were analysed by western blots. The results are expressed as the mean ± SD. *p < 0.05

Back to article page