Establishment of Cytarabine-resistant Acute Lymphoblastic Leukemia Cell Lines and Its Resistance Mechanism.
10.19746/j.cnki.issn.1009-2137.2021.05.006
- Author:
Xiang QIN
1
;
Jing LIU
1
;
Xi CHEN
1
;
Fang-Fang ZHONG
1
;
You YANG
1
;
Yan ZENG
1
;
Cheng LI
1
;
Wen-Jun LIU
2
Author Information
1. Department of Pediatrics, The Affiliated Hospital of Southwest Medical University; Sichuan Clinical Research Center for Birth Defects, Luzhou 646000, Sichuan Province, China.
2. Department of Pediatrics, The Affiliated Hospital of Southwest Medical University; Sichuan Clinical Research Center for Birth Defects, Luzhou 646000, Sichuan Province, China E-mail: lwjlyfy@qq.com.
- Publication Type:Journal Article
- MeSH:
ATP Binding Cassette Transporter, Subfamily G, Member 2;
Cell Line;
Cytarabine/pharmacology*;
Drug Resistance, Neoplasm;
Humans;
Neoplasm Proteins;
Precursor Cell Lymphoblastic Leukemia-Lymphoma
- From:
Journal of Experimental Hematology
2021;29(5):1403-1410
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To establish cytarabine-resistant acute lymphoblastic leukemia (ALL) cell lines and investigate its possible resistant mechanism.
METHODS:Low-concentration cytarabine (Ara-C) continuously induced and cultured Jurkat and Nalm-6 cells to construct cytarabine-resistant cell lines Jurkat/Ara-C and Nalm-6/Ara-C. The cell viability was detected by CCK-8 assay, and the distribution of cell cycle was detected by flow cytometry. Real-time fluorescence quantitative PCR was used to detect the mRNA expression levels of multidrug resistant gene and Ara-C metabolic enzymes. The expression levels of cyclin were detected by Western blot.
RESULTS:Jurkat/Ara-C and Nalm-6/Ara-C drug-resistant cell lines were successfully established, the resistance index of which was 1 973.908±161.163 and 7 231.643± 1 190.624, respectively. Drug-resistant cell lines had no cross-resistance to commonly used chemotherapeutic drugs, such as doxorubicin. Flow cytometry showed that the ratio of G
CONCLUSION:Cytarabine-resistant ALL cell lines are successfully established by using low concentration continuous induction method, and its drug-resistant mechanism may be related to the deficiencies of DCK and cyclinB1.
