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[MiR-30b Regulates the Cisplatin-Resistance of Human NK/T Cell Lypnphoma Cell Lines SNK-6 and YTS by Targeting the
Jian-Hong Wang1, Fang Liu1, Xiao-Hui Duan1
1Department of Hematology, Xijing Hospital, Air Force Medical University of PLA, Xi'an, 710032, Shaanxi Province, China.
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.
Insights
MicroRNA-30b (miR-30b) inhibits cisplatin resistance in human NK/T cell lymphoma by targeting CCL22. Lower miR-30b and higher CCL22 correlate with resistance, suggesting therapeutic potential.
Area of Science:
- Molecular Biology
- Oncology
- Immunology
Background:
- Cisplatin resistance is a major challenge in treating human NK/T cell lymphoma.
- The role of microRNAs in chemoresistance is an emerging area of research.
Purpose of the Study:
- To investigate the role and mechanism of miR-30b in cisplatin resistance in human NK/T cell lymphoma cell lines (SNK-6 and YTS).
Main Methods:
- Real-time PCR and Western blot were used to assess miR-30b and CCL22 expression.
- Cell viability, apoptosis, and caspase-3 activity were measured using MTT, flow cytometry, and assay kits.
- Dual-luciferase reporter assays confirmed the targeting relationship between miR-30b and CCL22.
Main Results:
- SNK-6 and YTS cells showed decreased miR-30b and increased CCL22 expression compared to normal NK cells.
- miR-30b mimics reduced cell viability, cisplatin resistance, and increased apoptosis and caspase-3 activity.
- miR-30b directly targets CCL22, and CCL22 overexpression reversed the effects of miR-30b mimics.
Conclusions:
- MiR-30b plays a crucial role in inhibiting cisplatin resistance in human NK/T cell lymphoma.
- The mechanism involves the direct targeting of CCL22 by miR-30b.
