The Effect of hnRNPK/Beclin1 Signaling on the Drug Resistance of Imatinib in Ph+ Leukemia.
10.19746/j.cnki.issn.1009-2137.2022.03.014
- Author:
Jin-Fang ZHANG
1
;
Xiao-Li LIU
2
;
Sa ZONG
3
Author Information
1. Department of Paediatric Hematology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, Guangdong Province, China,E-mail: jinfangzhang1216@126.com.
2. Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
3. Department of Paediatric Hematology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, Guangdong Province, China.
- Publication Type:Journal Article
- Keywords:
Beclin1;
autophagy;
drug resistance;
hnRNPK;
imatinib;
leukemia
- MeSH:
Antineoplastic Agents/pharmacology*;
Beclin-1;
Cell Line, Tumor;
Drug Resistance;
Drug Resistance, Neoplasm;
Heterogeneous-Nuclear Ribonucleoprotein K;
Humans;
Imatinib Mesylate/pharmacology*;
Leukemia
- From:
Journal of Experimental Hematology
2022;30(3):750-754
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effect of hnRNPK/Beclin1 signaling on the drug resistance of imatinib in Ph+ leukemia.
METHODS:Expression level of hnRNPK was verified in the imatinib resistant and sensitive Ph+ leukemia cell lines by using Western blot. hnRNPK expression was down-regulated by using RNAi. Expression level of LC3I/II and Beclin1 were detected by Western blot and the sensitivity of imatinib was analyzed by CCK-8 assay before and after modulation of hnRNPK expression.
RESULTS:hnRNPK showed overexpressed in imatinib resistant leukemia cell line. After the expression level of hnRNPK was down-regulated by RNAi, the sensitivity of drug resistance lines to imatinib restored, while the expression level of LC3I/II and Beclin1 were consistant with the modulation of hnRNPK expression.
CONCLUSION:hnRNP K/Beclin1 signaling may be involved in the development of imatinib resistance in Ph+ leukemia through the regulation of autophagy.
