| 宗桃梅,李其银,杨登权,等.蒲公英萜醇通过上调微小 RNA-610表达抑制鼻咽癌细胞的增殖、迁移侵袭[J].安徽医药,2022,26(12):2363-2367. |
| 蒲公英萜醇通过上调微小 RNA-610表达抑制鼻咽癌细胞的增殖、迁移侵袭 |
| Taraxacinol inhibits the proliferation, migration and invasion of nasopharyngeal carcinoma cells by up-regulating the expression of miR-610 |
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| DOI：10.3969/j.issn.1009-6469.2022.12.007 |
| 中文关键词: 鼻咽肿瘤 五环三萜类 细胞周期蛋白 D1 细胞周期蛋白质依赖激酶类 基质金属蛋白酶 9 基质金属蛋白酶 2 蒲公英萜醇 微小 RNA-610 增殖 迁移 侵袭 |
| 英文关键词: Nasopharyngeal neoplasms Pentacyclic triterpenes Cyclin D1 Cyclin-dependent kinases Matrix metallopro. teinase 9 Matrix metalloproteinase 2 Taraxerol MiR-610 Proliferation Migration Invasion |
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| 中文摘要: |
| 目的探讨蒲公英萜醇对鼻咽癌细胞增殖、迁移和侵袭的影响及分子机制。方法 2019年 4月至 2020年 1月，将鼻咽癌细胞 SUNE1分为对照组、蒲公英萜醇低、中、高浓度组、微小 RNA(miR)-NC组、 miR-610组、蒲公英萜醇 +anti-miR-NC组、蒲公英萜醇 +anti-miR-610组。 MTT法检测 SUNE1细胞增殖；蛋白质印迹法检测细胞周期蛋白依赖性激酶抑制剂 1A(p21)、细胞周期蛋白 D1(cyclin D1)、基质金属蛋白酶( MMP)-2、MMP-9蛋白表达； Transwell检测细胞迁移和侵袭；实时荧光定量 PCR(RT-qPCR)检测 miR-610表达水平。结果不同浓度蒲公英萜醇处理鼻咽癌细胞 SUNE1后，细胞增殖抑制率［( 16.72±1.42)%、(31.95±2.95)%、(54.59±5.0)%比( 0.00±0.00)%］和 p21、miR-610(1.68±0.14、2.37±0.21、3.09±0.29比 1.00±0.06)表达水平升高，迁移( 70.02±5.72、56.49±5.35、43.37±4.19比 86.71±7.05)、侵袭( 50.70±4.41、39.12±3.89、26.28±2.78比 69.12±4.80)细胞数和 Cy. clinD1、MMP-2、MMP-9水平降低，呈浓度依赖性( P<0.05)。过表达 miR-610可提高细胞增殖抑制率［( 46.66±4.48)%比( 7.11±0.74)%］和 p21表达水平，降低迁移( 52.18±5.35比 87.40±6.86)、侵袭( 33.11±3.29比 70.27±5.39)细胞数和 CyclinD1、MMP-2、 MMP-9表达水平(P<0.05)。抑制 miR-610表达逆转了蒲公英萜醇抗鼻咽癌 SUNE1细胞增殖、迁移和侵袭作用。结论蒲公英萜醇可抑制鼻咽癌细胞的增殖、迁移和侵袭，其机制可能与上调 miR-610表达相关。 |
| 英文摘要: |
| Objective To investigate the effect and molecular mechanism of taraxerol on the proliferation, migration and invasion ofnasopharyngeal carcinoma cells.Methods From April 2019 to January 2020, the nasopharyngeal cancer cell SUNE1 was divided intocontrol group, taraxerol low, medium and high concentration group, microRNA (miR)-NC group, miR-610 group, taraxerol+anti-miR-NC group, taraxerol+anti-miR-610 groups. MTT method was used to detect the proliferation of SUNE1 cells; Western blot method was used to detect cyclin-dependent kinase inhibitor 1A (p21), cyclin D1, matrix metalloproteinase (MMP)-2 and MMP-9 protein expres. sion; Transwell method was used to determine cell migration and invasion; real-time fluorescence quantitative PCR (RT-qPCR) was used to detect miR-610 expression.Results After treating nasopharyngeal carcinoma cell SUNE1 with different concentrations oftaraxerol, the cell proliferation inhibition rate [(16.72±1.42)%, (31.95±2.95)%, (54.59±5.0)% vs. (0.00±0.00)%] and the expression of p21, miR-610 (1.68±0.14, 2.37±0.21, 3.09±0.29 vs. 1.00±0.06) were increased, the number of migrating (70.02±5.72, 56.49±5.35, 43.37±4.19 vs. 86.71±7.05) and invasive (50.70±4.41, 39.12±3.89, 26.28±2.78 vs. 69.12±4.80) cells, and the expression levels of Cy. clinD1, MMP-2 and MMP-9 were decreased, all in a concentration-dependent manner (P<0.05). Overexpression of miR-610 increased the cell proliferation inhibition rate [(46.66±4.48)% vs. (7.11±0.74)%] and the expression level of p21, and reduced the number of mi. grated (52.18±5.35 vs. 87.40±6.86) and invasive (33.11±3.29 vs. 70.27±5.39) cells, and the expression levels of CyclinD1, MMP-2, and MMP-9 were decreased (P<0.05). Inhibition of miR-610 expression reversed the anti-proliferation, migration and invasion effects of taraxerol on nasopharyngeal carcinoma SUNE1 cells.Conclusion Taraxerol can inhibit the proliferation, migration and invasion of na.sopharyngeal carcinoma cells, and the mechanism may be related to the up-regulating of miR-610 expression. |
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