| 引用本文:黄渊智，刘红玲.芒柄花素通过miR-1229/ZDHHC9分子轴对胶质瘤细胞增殖、活力及凋亡的影响[J].世界中医药,2024,(03):. |
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| 芒柄花素通过miR-1229/ZDHHC9分子轴对胶质瘤细胞增殖、活力及凋亡的影响 |
| Effects of Formononetin on Proliferation，Viability，and Apoptosis of Glioma Cells by Regulating the Molecular Axis of MiR-1229/ZDHHC9 |
| 投稿时间：2023-09-19 |
| DOI：10.3969/j.issn.1673-7202.2024.03.006 |
| 中文关键词: 芒柄花素 胶质瘤 微小核糖核酸-1229 棕榈酰化转移酶9 细胞增殖 细胞凋亡 移植瘤 分子机制 |
| English Keywords:Formononetin Glioma MiR-1229 ZDHHC9 Cell proliferation Cell apoptosis Subcutaneous tumor transplantation Molecular mechanism |
| 基金项目:广西壮族自治区卫生厅自筹经费项目（Z2013740）——广西钦州沿海地区缺血性脑卒中发病危险因素调查 |
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| 中文摘要: |
| 目的：探讨芒柄花素对胶质瘤细胞增殖和凋亡的影响及其分子作用机制。方法：构建皮下移植瘤小鼠模型，灌胃给予5.72、14.31、22.9、31.49 mg/kg剂量的芒柄花素，观察肿瘤重量、体积变化；免疫组织化学法检测肿瘤组织增殖细胞核抗原（PCNA）表达。用不同浓度（20、50、80、110 μmol/L）的芒柄花素处理TJ905细胞，并将TJ905细胞分为空白对照组、110 μmol/L芒柄花素组、110 μmol/L芒柄花素+miR-1229组、110 μmol/L芒柄花素+miR-1229+ZDHHC9组、miR-NC组、miR-1229 mimic组。用Edu实验、CCK-8实验检测细胞增殖能力，TUNEL实验检测细胞凋亡，实时荧光定量聚合酶链反应(RT-qPCR)实验检测miR-1229、ZDHHC9 mRNA表达水平，在线网站及双荧光素酶报告基因法验证miR-1229与ZDHHC9靶向结合。结果：与空白对照组比较，不同剂量的芒柄花素处理组肿瘤体积、重量及PCNA蛋白表达均显著降低（均P<0.05）。与对照组比较，不同浓度（20、50、80、110 μmol/L）的芒柄花素处理后，细胞增殖率显著降低，凋亡率显著升高（均P<0.05）；与110 μmol/L芒柄花素组比较，110 μmol/L芒柄花素+miR-1229组细胞增殖率、细胞活力均显著降低，凋亡率显著增加（均P<0.05）；与110 μmol/L芒柄花素+miR-1229组比较，110 μmol/L芒柄花素+miR-1229+ZDHHC9组细胞增殖率、细胞活力均显著增加，凋亡率显著下降（均P<0.05）；双荧光素酶报告基因实验验证miR-1229与ZDHHC9靶向结合。结论：芒柄花素可能通过miR-1229/ZDHHC9分子轴抑制胶质瘤细胞增殖，并诱导其凋亡。 |
| English Summary: |
| To investigate the effect of formononetin on the proliferation and apoptosis of glioma cells and its molecular mechanism.Methods:A subcutaneous xenograft tumor mouse model was established，and mice were orally administered with formononetin at 5.72，14.31，22.9，and 31.49 mg/kg.Tumor weight and volume changes were observed，and the expression of proliferating cell nuclear antigen(PCNA) in tumor tissues was detected using immunohistochemistry.TJ905 cells were treated with different concentrations(20，50，80，and 110 μmol/L) of formononetin，and the cells were divided into blank control group，110 μmol/L formononetin group，110 μmol/L formononetin+miR-1229 group，110 μmol/L formononetin+miR-1229+ZDHHC9 group，miR-NC group，and miR-1229 mimic group.Cell proliferation ability was detected using Edu assay and CCK-8 assay.Cell apoptosis was detected using TUNEL assay.The expression levels of miR-1229 and ZDHHC9 mRNA were measured using real-time fluorescence quantitative polymerase chain reaction(RT-qPCR) assay.The targeting binding of miR-1229 to ZDHHC9 was verified using online websites and dual luciferase reporter gene assay.Results:Compared with the blank control group，the tumor volume，weight，and PCNA protein expression in the formononetin-treated groups at different doses were significantly reduced(all P<0.05).Compared with the control group，treatment with different concentrations(20，50，80，and 110 μmol/L) of formononetin significantly reduced cell proliferation rate and increased apoptosis rate(all P<0.05).Compared with the 110 μmol/L formononetin group，the cell proliferation rate and viability in the 110 μmol/L formononetin+miR-1229 group were significantly reduced，and the apoptosis rate was significantly increased(all P<0.05).Compared with the 110 μmol/L formononetin+miR-1229 group，the cell proliferation rate and viability in the 110 μmol/L formononetin+miR-1229+ZDHHC9 group were significantly increased，and the apoptosis rate was significantly decreased(all P<0.05).The dual luciferase reporter gene assay confirmed the targeted binding of miR-1229 to ZDHHC9.Conclusion:Formononetin may inhibit the proliferation of glioma cells and induce their apoptosis through the miR-1229/ZDHHC9 molecular axis. |
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