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
,
2
;
Jing LIU
1
,
2
;
Xi CHEN
1
,
2
;
Fang-Fang ZHONG
1
,
2
;
You YANG
1
,
2
;
Yan ZENG
1
,
2
;
Cheng LI
1
,
2
;
Wen-Jun LIU
1
,
3
Author Information
1. Department of Pediatrics, The Affiliated Hospital of Southwest Medical University
2. Sichuan Clinical Research Center for Birth Defects, Luzhou 646000, Sichuan Province, China.
3. 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.
