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.
Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Chemokine CCL22 , Cisplatin , Gene Expression Regulation, Neoplastic , Killer Cells, Natural , Lymphoma, T-Cell , Genetics , MicroRNAs , T-LymphocytesABSTRACT
<p><b>OBJECTIVE</b>To investigate the influence of the diameter and length of the mini-implant on the primary stability after loading with composite forces (CF) which contained torque and horizontal forces (HF).</p><p><b>METHODS</b>Ninety-six finite element models were established by the combination of mini-implant and bone, diameters (1.2 mm, 1.6 mm, 2.0 mm) and length (6 mm, 8 mm, 10 mm, 12 mm). There were 12 sizes, each size corresponded with 8 models. Group HF (each size n = 4) was loaded with 1.96 N horizontal force and Group CF (each size n = 4) was loaded with composite force which contained 6 N·mm torque and 1.96 N horizontal force. The maximum displacement of mini-implant with different force directions, implant diameters and lengths were evaluated.</p><p><b>RESULTS</b>The effect of force direction on the displacement related to diameter of mini-implant. The maximum displacement under load with HF respectively was changed with the changing of diameter[1.2 mm: (7.71 ± 0.49) µm; 1.6 mm: (3.94 ± 0.31) µm; 2.0 mm: (2.32 ± 0.43) µm], which were smaller than the maximum displacement of Group CF [1.2 mm: (9.22 ± 0.63) µm; 1.6 mm: (4.62 ± 0.52) µm; 2.0 mm: (2.69 ± 0.49) µm] (P < 0.05). When diameter was 1.2 mm, the difference of the maximum displacement [(1.61 ± 0.22) µm] between Group HF and CF was more obvious than that when the diameter was 1.6 mm or 2.0 mm [(0.64 ± 0.12), (0.49 ± 0.06) µm] (P < 0.05).</p><p><b>CONCLUSIONS</b>The composite force had unfavorable effect on the primary stability of the mini-implant. The diameter of the mini-implant had better be larger than 1.2 mm when the composite forces were applied.</p>