目的：探讨紫甘薯花色苷（purple sweet potato anthocyanin, PSPA）是否通过 circ_0003998/miR-145 轴调控乳腺癌 MDA-MB-231细胞的增殖、迁移和侵袭。方法：选用乳腺癌MDA-MB-231细胞，将其分为对照组，200、400和800 μg/ml PSPA 组，pcDNA 组、pcDNA-circ_0003998 组、si-NC 组、si-circ_0003998 组、si-circ_0003998+anti-miR-145 组、PSPA+pcDNA 组、PSPA+ pcDNA-circ_0003998 组和 PSPA+anti-miR-145 组。用 qPCR 法检测细胞中 circ_0003998 和 miR-145 的表达，CCK-8 法、Transwell 小室法分别检测转染前后细胞的增殖、迁移和侵袭能力，WB法检测细胞中Ki-67、MMP-2 和 MMP-9 蛋白的表达。用双荧光素 酶报告基因实验验证circ_0003998与miR-145 的靶向关系。结果：与对照组比较，各剂量PSPA组 MDA-MB-231细胞的增殖抑 制率、miR-145表达水平均显著升高（均P<0.01）Ki-67、MMP-2、MMP-9蛋白和circ_0003998的表达水平、细胞迁移和侵袭细胞数 均显著降低（均P<0.01），并呈现浓度依赖性。circ_0003998可以靶向负调控miR-145的表达。敲减circ_0003998后，MDA-MB-231细 胞的增殖抑制率、miR-145表达水平显著升高，Ki-67、MMP-2 和 MMP-9 蛋白表达水平、细胞迁移和侵袭细胞数均显著减少（均P<0.01）。共转染si-circ_0003998和anti-miR-145则可逆转敲减circ_0003998表达对MDA-MB-231细胞增殖、迁移和侵袭的抑制 作用，过表达circ_0003998或抑制miR-145表达可逆转PSPA对MDA-MB-231细胞增殖、迁移和侵袭的抑制作用。结论：PSPA通 过circ_0003998/miR-145轴抑制乳腺癌MDA-MB-231细胞的增殖、迁移和侵袭。
Objective: To investigate whether purple sweet potato anthocyanin (PSPA) regulates the proliferation, migration and invasion of breast cancer MDA-MB-231 cells through the circ_0003998/miRNA-145 axis. Methods: Breast cancer MDA-MB-231 cells were divided into control group, PSPA groups (200, 400, 800 μg/ml PSPA), pcDNA group, pcDNA-circ_0003998 group, si-NC group, si-circ_0003998 group, si-circ_0003998+anti-miR-145 group, PSPA+pcDNA group, PSPA+pcDNA-circ_0003998 group and PSPA+anti-miR-145 group. The expressions of circ_0003998 and miR-145 in MDA-MB-231 cells were detected by qPCR method. The cell proliferation, migration and invasion abilities were measured by CCK-8 method and Transwell chamber method, respectively. WB was used to detect the protein expressions of Ki-67, MMP-2 and MMP-9 in cells. Dual luciferase reporter gene assay was used to analyze the targeting relationship between circ_0003998 and miR-145. Results: Compared with the control group, the proliferation inhibition rate and miR-145 expression level in MDA-MB-231 cells of various PSPA groups increased significantly, while the expression of circ_0003998 and protein expression levels of Ki-67, MMP-2, MMP-9, as well as the number of migrated and invaded cells were significantly reduced (all P<0.01), all of which were in a concentration-dependent manner. circ_0003998 could target and negatively regulate the expression of miR-145. After inhibiting circ_0003998, the proliferation inhibition rate and the expression level of miR-145 in MDA-MB-231 cells were significantly increased, while the protein expression levels of Ki-67, MMP-2 and MMP-9, and the number of migrated and invaded cells were significantly reduced (all P<0.01). After co-transfection of si-circ_0003998 and anti-miR-145, the suppression effect of circ_0003998 inhibition on the proliferation, migration and invasion of MDA-MB-231 cells were reversed. circ_0003998 overexpression or miR-145 inhibition could reverse the inhibitory effects of PSPA on the proliferation, migration and invasion of MDA-MB-231 cells. Conclusion: PSPA inhibites the proliferation, migration and invasion of breast cancer MDA-MB-231 cells through the circ_0003998/miR-145 axis.