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南京医科大学学报(自然科学版)                                  第41卷第2期
               ·198 ·                     Journal of Nanjing Medical University(Natural Sciences)   2021年2月


             ·基础研究·

              circ_0001246 调节 miRNA30a 对骨肉瘤化疗敏感性影响的机制

              研究



              王   娟 ,吴 涛 ,何        斌 ,王伯尧 ,魏新程 ,范          磊  2*
                                     2
                                             2
                     1
                                                     2
                             2
                                           2
              1 南京医科大学第二附属医院超声科,骨科,江苏                南京 210011
             [摘    要] 目的:探讨circ_0001246调节miRNA30a及影响骨肉瘤化疗敏感性的机制。方法:将骨肉瘤细胞随机分为3组,分
              别置于6孔板中,包括未转染组(空白组)、siRNA阴性对照转染组(NC组)和siRNA转染组(circ_0001246 siRNA转染组),转染
              后荧光倒置显微镜观察转染效率,检测各组细胞circ_0001246、miRNA30a的表达,用流式细胞AnnexinV/7AAD双染法检测各
              组细胞对化疗药物依托泊苷(etoposide ⁃VP16)的敏感性,荧光素酶报告基因实验验证 circ_0001246 对 miRNA30a 的“吸附”作
              用。结果:circ_0001246 siRNA转染组的细胞miRNA30a表达较NC组和空白组明显上调(P < 0.05),骨肉瘤中circ_0001246和
              miRNA30a 的表达呈现负反馈。circ_0001246 siRNA 转染组细胞凋亡率较 NC 组和空白组明显升高(P < 0.05)。circ_0001246
              可以通过直接碱基配对吸附 miRNA30a 发挥调控作用。结论:circ_0001246 是骨肉瘤相关癌基因,靶向抑制骨肉瘤中 circ_
              0001246表达可以增强肿瘤细胞对化疗药物依托泊苷的敏感性,该作用可能是通过circ_0001246的吸附功能负调控miRNA30a
              表达而实现的。
             [关键词] circ_0001246;miRNA30a;化疗;依托泊苷;骨肉瘤
             [中图分类号] R738.1                   [文献标志码] A                        [文章编号] 1007⁃4368(2021)02⁃198⁃05
              doi:10.7655/NYDXBNS20210208



              The mechanism of effect of circ_0001246 on osteosarcoma chemotherapy sensitivity by
              regulating miRNA31a
                        1        2       2            2             2       2*
              WANG Juan ,WU Tao ,HE Bin ,WANG Boyao ,WEI Xincheng ,FAN Lei
                                             2
              1 Department of Ultrasonic Diagnosis,Department of Orthopedics,the Second Affiliated Hospital of Nanjing Medical
              University,Nanjing 210011,China


             [Abstract] Objective:This study aims to investigate the molecular mechanism of osteosarcoma chemotherapy sensitivity regulation
              of circ_0001246 via targeting miRNA30a. Methods:The MG63 and U2OS cells were randomly allocated into three groups in 6⁃well
              plates respectively,including non⁃transfection group(blank group),siRNA negative control transfection group(NC group),and siRNA
              transfection group(circ_0001246 siRNA). The transfection efficiencies were evaluated by fluorescence inverted microscope.
              Expression Level of circ_0001246 and miRNA30a were detected. Osteosarcoma chemotherapy sensitivity were detected by annexin V⁃
              FITC/7AAD apoptosis double staining. Function of circ_0001246 to adsorb miRNA30a were verified by luciferase reporter gene assay.
              Results:MiRNA30a expression in the circ_0001246 siRNA transfection group were significantly up⁃regulated compared to the NC
              group and blank group(P < 0.05). We found circ_0001246 and miRNA30a were inversely expressed. Osteosarcoma chemotherapy
              sensitivity in the circ_0001246 siRNA transfection group were significantly up⁃regulated compared to the NC group and blank group
             (P < 0.05). circ_0001246 could adsorb miRNA30a by direct base pairs. Conclusion:Circ_0001246 is an osteosarcoma related
              oncogene. Targeted inhibition of circ_0001246 expression in osteosarcoma can enhance the chemotherapy sensitivity of tumor cells to
              etoposide⁃VP16. One of the mechanisms is the negative regulation of the miRNA30a expression by the adsorption function of circ_
              0001246.
             [Key words] circ_0001246;miRNA30a;chemotherapy;etoposide;osteosarcoma
                                                                            [J Nanjing Med Univ,2021,41(02):198⁃202]
             [基金项目] 江苏省自然科学青年基金(BK20171092)
              ∗
              通信作者(Corresponding author),E⁃mail:fanlei8839@126.com
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