山奈素通过下调circ-RPL15抑制肺癌细胞A549的增殖和迁移

目的：探索山奈素是否通过circ-RPL15 影响肺癌细胞A549 的生物行为。方法：使用25、50 和75 μg/mL山奈素处理肺癌细胞A549。在细胞A549中沉默circ-RPL15，或过表达circ-RPL15并使用75 μg/mL山奈素处理。采用细胞计数试剂盒8（CCK-8）检测各组肺癌细胞A549 活力变化，平板克隆法检测细胞克隆形成，流式细胞术检测细胞凋亡，蛋白质印迹（Western blot）法检测裂解-含半胱氨酸的天冬氨酸蛋白水解酶3（Cleaved-caspase3）蛋白的表达，使用Transwell法检测细胞迁移，并使用实时定量聚合酶链反应（RT-qPCR）检测circ-RPL15、miR-489-3p表达。双荧光素酶报告实验分析circ-RPL15对miR-489-3p的靶向调控。结果：与对照组相比，不同质量浓度（25、50 和75 μg/mL）山奈素作用于肺癌细胞A549 后，细胞活力、克隆形成数、迁移数、circ-RPL15表达量降低，而凋亡率、Cleaved-caspase3蛋白和miR-489-3p的表达量升高（P ＜0.05），且均呈浓度依赖性。沉默circ-RPL15 增强肺癌细胞A549 的miR-489-3p表达量、凋亡率和Cleaved-caspase3蛋白的表达量，并减弱细胞活力、克隆形成数、迁移数（P ＜0.05）。circ-RPL15靶向调控miR-489-3p。过表达circ-RPL15逆转了山奈素作用的肺癌细胞增殖、凋亡和迁移情况（P ＜0.05）。结论：山奈素通过下调circ-RPL15并靶向调控miR-489-3p，抑制肺癌细胞的增殖和迁移，并诱导其凋亡。

Kaempferide inhibits the proliferation and migration of lung cancer cell A549 by down-regulating circ-RPL15

Objective: To explore whether kaempferide can affect the biological behavior of lung cancer cell A549 through circ-RPL15. Methods: Kaempferide of 25, 50, and 75 μg/mL was used to treat lung cancer cells A549. The dual luciferase report experiment was used to analyze the targeted regulation of miR-489-3p by circ-RPL15. circ-RPL15 was silenced or overexpressed in cell A549, and treated with 75 μg/mL kaempferol. Cell counting kit-8 (CCK-8) was applied to measure changes in the viability of lung cancer cells A549 in each group;plate cloning was performed to detect cell clone formation; flow cytometry was used to monitor cell apoptosis;Western blot was employed to detect the expression of Cleaved-caspase3 protein; Transwell method was used to detect cell migration, and real-time quantitative polymerase chain reaction (RT-qPCR) to determine the expression of circ-RPL15 and miR-489-3p. The dual luciferase report experiment analyzed the targeted regulation of miR-489-3p by circ-RPL15. Results: Compared with the control group, after different concentrations (25, 50 and 75 μg/mL) of kaempferide acted on lung cancer cell A549, cell viability, clone formation number, migration number and circ-RPL15 expression decreased, while apoptosis rate, Cleaved-caspase3 protein and miR-489-3p expression increased (P<0.05), and all were concentration-dependent. Silencing circ-RPL15 enhanced the expression of miR-489-3p, apoptosis rate and Cleaved-caspase3 protein expression of lung cancer cell A549, and weakened cell viability, the number of clone formation, and the number of migration (P<0.05). circ-RPL15 targets miR-489-3p. Overexpression of circ-RPL15 reversed the proliferation, apoptosis and migration of lung cancer cells that were affected by kaempferide (P<0.05). Conclusion: Kaempferide inhibits the proliferation and migration of lung cancer cells and induces their apoptosis by down-regulating circ-RPL15 and targeting miR-489-3p.