[目的]探讨miR-492调控Smad2/TGF-β对骨髓增生异常综合征SKM-1细胞地西他滨药物敏感性的影响。[方法]设立 SKM-1 细胞组、miR-NC 组、miR-492 低表达(inhibitor)组、地西他滨(Docetaxel)组、miR-492 inhibitor+Docetaxel组。各组进行相应干预后，测定SKM-1细胞增殖、克隆形成数目、凋亡、侵袭水平、miR-492、Smad2、TGF-β基因和蛋白水平。[结果]SKM-1细胞组与miR-NC组各指标比较差异无统计学意义(P＞0。05)。与SKM-1细胞组和 miR-NC 组比较，miR-492 inhibitor 组、Docetaxel 组、miR-492 inhibitor+Docetaxel 组存活率、细胞克隆形成数、穿膜数、miR-492、Smad2 mRNA及蛋白、TGF-β mRNA及蛋白表达水平降低，凋亡率升高(P＜0。05)。miR-492 inhibitor组和Docetaxel组比较各指标差异无统计学意义(P＞0。05)。[结论]miR-492低表达通过靶向沉默Smad2(1。39±0。12、1。56±0。19 vs 0。85±0。11、0。86±0。10、0。34±0。10)/TGF-β(1。49±0。13、1。46±0。14 vs 0。81±0。12、0。80±0。10、0。52±0。13)信号通路抑制骨髓增生异常综合征SKM-1细胞恶性生物学行为，增强SKM-1细胞对地西他滨的敏感性。
Mechanism of miR-492 targets and silences Smad2 to enhance the sensitivity of SKM-1 cells to decitabine
[Objective]To explore the effect of between psychological status and coping style,self-efficacy and quality of life in cancer patients.[Method]SKM-1 cell group,miR-NC group,miR-492 low expression(inhibitor)group,decitabine(Docetaxel)group and miR-492 inhibitor+Docetaxel group were established.After the corresponding intervention in each group,SKM-1 cell proliferation,number of clone formation,apoptosis and invasion levels were determined,and the levels of miR-492,Smad2 and TGF-β genes and proteins were explored by RT-PCR and Western Blot.[Result]There was no statis-tically significant difference in various indicators between the SKM-1 cell group and the miR-NC group(P＞0.05).Com-pared with the SKM-1 cell group and the miR-NC group,the survival rate,cell colony formation number,membrane penetra-tion number,miR-492,Smad2 mRNA and protein,The expression levels of TGF-β mRNA and protein decreased,and the ap-optosis rate increased(P＜0.05).There was no statistically significant difference in various indicators between the miR-492 inhibitor group and the Docetaxel group(P＞0.05).[Conclusion]Low expression of miR-492 through targeted silencing of Smad2(1.39±0.12,1.56±0.19 vs 0.85±0.11,0.86±0.10,0.34±0.10)/TGF-β(1.49±0.13,1.46±0.14 vs 0.81±0.12,0.80±0.10,0.52±0.13)signaling pathway inhibits the malignant biological behavior of myelodysplastic syndrome SKM-1 cells and enhances the sensitivity of SKM-1 cells to decitabine.
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