miR-492靶向沉默Smad2增强SKM-1细胞对地西他滨药物敏感性的机制  

Mechanismof miR-492 targets and silences Smad2 to enhance the sensitivity of SKM-1 cells to decitabine

作　　者：王友君 李素欣 冯丽倩 王苗 李栋梁 安乐 文文 WANG Youjun;LI Suxin;FENG Liqian;WANG Miao;LI Dongliang;AN Le;WEN Wen(Department of Hematology,Shijiazhuang People′s Hospital,Shijiazhuang 050000;Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine,Cangzhou 061000,China)

机构地区：[1]石家庄市人民医院血液内科,河北石家庄050000 [2]河北省沧州中西医结合医院,河北沧州061000

出　　处：《生物技术》2024年第6期735-741,787,共8页Biotechnology

基　　金：河北省2022年度医学科学研究课题计划项目(20221711)。

摘　　要：[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-βmRNA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。[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-βgenes 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-βmRNA 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.

关 键 词：miR-492 SMAD2 TGF-β 通路 骨髓增生异常综合征 SKM-1细胞 地西他滨 药物敏感 

分 类 号：Q784[生物学—分子生物学]