目的：探讨鱼藤素通过调控miR-520a-3p表达对卵巢癌SKOV3细胞增殖和凋亡的影响。方法：将SKOV3细胞分为对照组（鱼藤素0 μmol/L）、鱼藤素低剂量（5 μmol/L）、中剂量（10 μmol/L）、高剂量（20 μmol/L）组，miR-NC 组、过表达miR-520a-3p组，鱼藤素+anti-miR-NC 组、鱼藤素+anti-miR-520a-3p组。CCK-8法、细胞集落形成实验、FCM以及qPCR 法分别检测SKOV3细胞的增殖抑制率、细胞克隆形成数、凋亡率以及miR-520a-3p表达水平。结果：与对照组比较，鱼藤素（低、中、高剂量）组SKOV3细胞增殖抑制率、凋亡率、miR-520a-3p 表达水平均显著升高（均P<0.05），细胞克隆形成数显著减少（P<0.05）。与miR-NC 组比较，过表达miR-520a-3p组SKOV3细胞的增殖抑制率、凋亡率均显著升高（均P<0.05），细胞克隆形成数显著减少（P<0.05）。与鱼藤素+anti-miR-NC 组比较，鱼藤素+anti-miR-520a-3p 组SKOV3 细胞的增殖抑制率、凋亡率均显著降低（均P<0.05），细胞克隆形成数显著增多（P<0.05）。结论：鱼藤素通过增加miR-520a-3p表达抑制卵巢癌SKOV3细胞的增殖能力，并诱导其凋亡。

Objective: To investigate the effects of deguelin on the proliferation and apoptosis of ovarian cancer SKOV3 cells by regulating miR-520a-3p. Methods: The SKOV3 cells were divided into the control group (deguelin 0 μmol/L), low-dose deguelin group (5 μmol/L), medium-dose deguelin group (10 μmol/L), and high-dose deguelin group (20 μmol/L), miR-NC group, miR-520a-3p group, deguelin+anti-miR-NC group and deguelin+anti-miR-520a-3p group. CCK-8, colony formation experiment, flow cytometry and qPCR were used to detect the inhibition rate, the number of clone formation, the apoptosis rate and the miR-520a-3p expression of SKOV3 cells respectively. Results: Compared with the control group, the inhibition rate, the apoptosis rate, miR-520a-3p expression of SKOV3 cells in the deguelin (low, medium, and high dose) groups were significantly increased (all P<0.05), and the number of clone formation was significantly reduced (P<0.05). Compared with the miR-NC group, the inhibitory rate and the apoptosis rate of SKOV3 cells in the miR-520a-3p group were significantly increased (all P<0.05), and the number of clone formation was significantly reduced (P<0.05). Compared with the deguelin+anti-miR-NC group, the inhibition rate and the apoptosis rate of SKOV3 cells in the deguelin+anti-miR-520a-3p group were significantly reduced (all P<0.05), and the number of clone formation was significantly increased (P<0.05). Conclusion: Deguelin inhibited the proliferation potential of ovarian cancer SKOV3 cells and induced cell apoptosis by increasing the expression of miR-520a-3p.