MiR-30b Regulates the Cisplatin-Resistance of Human NK/T Cell Lypnphoma Cell Lines SNK-6 and YTS by Targeting the CCL22.
10.19746/j.cnki.issn.1009-2137.2019.06.021
- Author:
Jian-Hong WANG
1
;
Fang LIU
1
;
Xiao-Hui DUAN
1
;
Cai-Xia HAO
1
;
Xiang-Xiang LIU
1
;
Ying-Juan LU
1
;
Zhe WANG
1
;
Rong LIANG
2
Author Information
1. Department of Hematology, Xijing Hospital, Air Force Medical University of PLA, Xi'an, 710032, Shaanxi Province, China.
2. Department of Hematology, Xijing Hospital, Air Force Medical University of PLA, Xi'an, 710032, Shaanxi Province, China E-mail: rongliang1071@yahoo.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Line, Tumor;
Cell Proliferation;
Chemokine CCL22;
Cisplatin;
Gene Expression Regulation, Neoplastic;
Humans;
Killer Cells, Natural;
Lymphoma, T-Cell;
genetics;
MicroRNAs;
T-Lymphocytes
- From:
Journal of Experimental Hematology
2019;27(6):1838-1844
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effect and mechanism of miR-30b on cisplatin-resistance of human NK/T cell lymphoma lines SNK-6 and YTS cells.
METHODS:Normal NK cells, SNK-6 and YTS cells were cultured, the expression levels of miR-30b and macrophage-derived chemokine (CCL22) were detected by real-time PCR assay, and the CCL22 expression was detected by Western blot. The SNK-6 and YTS cells were transfected with miR-30b mimics and inhibitor respectively, then the effect of cisplatin resistance in SNK-6 and YTS cells was measured by MTT assay, the activity of caspase-3 was detected by caspase-3 assay kit, and the cell apoptosis was analyzed by flow cytometry. Dual-luciferase reporter gene assay was used to determine the targeting relationship between miR-30b and CCL22. Furthermore, the effect of CCL22 on cisplatin-resistance and caspase-3 actirity was also evaluated.
RESULTS:Compared with the normal NK cells, the expression levels of miR-30b significantly decreased in both SNK-6 and YTS cells (P＜0.01), but CCL22 mRNA expression increase in both cells (P＜0.01). MiR-30b mimics decreased the cell activity (P＜0.05), down-regulated the cisplatin-resistance (P＜0.05), and increased cell apoptosis and caspase-3 activity (P＜0.05). The effects of miR-30b inhibitor were contrary to the mimics. Up-regulation of miR-30b expression significantly decreased the luciferase activity in CCL22 3'-UTR-transfected NK cells, but not in Mut-CCL22 3'UTR group, suggesting that CCL22 could act as a direct target of miR-30b. The expressions of CCL22 pathway proteins were down-regulated after SNK-6 cells transfected with miR-30b mimics (P＜0.05), while this effect was restored by overexpression of CCL22. Moreover, CCL22 overexpression also increased the cell activity and decreased caspase-3 activity when SNK-6 cells were transfected with miR-30b mimics.
CONCLUSION:MiR-30b inhibits cisplatin-resistance of human NK/TCL SNK-6 and YTS cells by targeting CCL22.
