| 张洪岩,刘 欢,朱宝杰,范宜锋.余甘子提取物调控LINC01772/miR-153对肺癌细胞A549生物学行为的影响[J].,2024,(5):841-848 |
| 余甘子提取物调控LINC01772/miR-153对肺癌细胞A549生物学行为的影响 |
| Effect of Phyllanthus Emblica Extract on the Biological Behavior of Lung Cancer Cell A549 by Regulating LINC01772 / miR-153 |
| 投稿时间：2023-09-04 修订日期：2023-09-30 |
| DOI：10.13241/j.cnki.pmb.2024.05.007 |
| 中文关键词: 余甘子提取物 肺癌 LINC01772 miR-153 细胞增殖 细胞迁移 细胞侵袭 |
| 英文关键词: Phyllanthus emblica extract Lung cancer LINC01772 miR-153 Cell proliferation Cell migration Cell invasion |
| 基金项目:河北省科学技术研究项目（20201217）；2018年廊坊市科技支撑计划项目（2018013158） |
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| 中文摘要: |
| 摘要 目的：探讨余甘子提取物对肺癌细胞A549增殖、迁移和侵袭的影响及机制。方法：体外培养A549细胞，分为对照组、不同剂量（低、中、高剂量）余甘子提取物组、si-NC组、si-LINC01772组、高剂量余甘子提取物+pcDNA组和高剂量余甘子提取物+pcDNA-LINC01772组，细胞计数试剂盒（CCK-8）法和克隆形成实验检测细胞增殖，划痕实验检测细胞迁移，嵌入式细胞共培养法（Transwell）检测细胞侵袭，免疫印迹法（Western Blot）检测细胞中上皮型钙黏蛋白（E-cadherin）和神经型钙黏蛋白（N-cadherin）蛋白表达水平，实时荧光定量PCR（RT-qPCR）检测LINC01772和miR-153表达水平。双荧光素酶报告基因实验验证LINC01772和miR-153调控关系。结果：与对照组相比，不同剂量余甘子提取物组A549细胞中LINC01772表达降低，且光密度值（OD值）、克隆形成数、迁移以及侵袭细胞数减少（P<0.05），而miR-153含量与E-cadherin蛋白表达升高（P<0.05），且呈剂量依赖性（P<0.05）。LINC01772在A549细胞中负调控miR-153表达。与si-NC组相比，si-LINC01772组A549细胞增殖，侵袭及迁移能力受到抑制（P<0.05）。与高剂量余甘子提取物+pcDNA组相比，高剂量余甘子提取物+pcDNA-LINC01772组A549细胞增殖，侵袭及迁移能力增强（P<0.05）。结论：余甘子提取物可能通过调控LINC01772/miR-153轴抑制肺癌细胞A549增殖、迁移和侵袭，其可能通过下调LINC01772进而上调miR-153表达发挥作用,具有开发为治疗肺癌药物的潜在价值。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect and mechanism of phyllanthus emblica extract on proliferation, migration and invasion of lung cancer cell A549. Methods: A549 cells were cultured in vitro and divided into control group, different doses (low, medium and high doses ) phyllanthus emblica extract group,si-NC group, si-LINC01772 group, high dose phyllanthus emblica extract+pcDNA group and high dose phyllanthus emblica extract+pcDNA-LINC01772 group. Cell proliferation was detected by cell counting kit-8 (CCK-8) and clone formation assay. Cell migration was detected by scratch assay. Cell invasion was detected by Transwell assay.The expression levels of E-cadherin and N-cadherin in the cells were detected by Western Blot, and the expression levels of LINC01772 and miR-153 were detected by real-time fluorescence quantitative PCR (RT-qPCR). The regulatory relationship between LINC01772 and miR-153 was verified through the dual luciferase reporter gene assay. Results: Compared with the control group, the expression of LINC01772 in A549 cells in different doses of phyllanthus emblica extract groups was decreased, and the optical density (OD value), number of clone formation, migration and invasion cells were decreased (P<0.05), while the content of miR-153 and the expression of E-cadherin protein were increased (P<0.05), with a dose-dependent manner (P<0.05). LINC01772 negatively regulated miR-153 expression in A549 cells. Compared with the si-NC group, the proliferation, invasion and migration of A549 cells in the si-LINC01772 group were inhibited (P<0.05). Compared with the high dose phyllanthus emblica extract+pcDNA group, the proliferation, invasion and migration of A549 cells in the high dose phyllanthus emblica extract+pcDNA-LINC01772 group were enhanced (P<0.05). Conclusion: Phyllanthus emblica extract may inhibit the proliferation, migration and invasion of lung cancer cell A549 by regulating the LINC01772/miR-153 axis, which may play a role by down-regulating LINC01772 and up-regulating the expression of miR-153, and has the potential value to be developed as a drug for the treatment of lung cancer. |
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