Cervical cancer (CC) is a common gynecological tumor, ranking second in the female reproductive system tumor. The work aims to study the function of miR-17-5p in the occurrence and pathogenesis of CC. We collected 36 cases of CC tissues for clinical analysis, and two CC cell lines (C33a and HCC94) were obtained for cellular analysis. As expected, the up-regulated miR-17-5p and down-regulated TIMP2 were detected in CC tissues and cell lines by RT-qPCR, in contrast with their normal counterparts. Then, overexpression of miR-17-5p significantly increased the CC cells viability and colonies formation abilities. Moreover, the Transwell analysis revealed that miR-17-5p promoted the capability of invasion and migration. Meanwhile, the expression levels of MMP2 and MMP9 was inhibited by the inhibition of miR-17-5p. The luciferase analysis demonstrated that TIMP2 was the target of miR-17-5p. In addition, cell proliferation, invasion and migration in HCC94 cells were repressed by silencing miR-17-5p, which were reversed by TIMP2 knockdown. In summary, all results indicated that miR-17-5p targeted TIMP2 to modulate CC cells’ proliferation, invasion and migration through MMPs signaling pathway; and the miR-17-5p/TIMP2/MMPs signaling pathway had the potential to become a therapeutic target of CC for clinical utilization.

宫颈癌（CC）是一种常见的妇科肿瘤，在女性生殖系统肿瘤中排名第二。本工作旨在研究miR-17-5p在CC发生及发病机制中的作用。我们收集了 36 例 CC 组织进行临床分析，获得了两个 CC 细胞系（C33a 和 HCC94）进行细胞分析。正如预期的那样，通过 RT-qPCR 在 CC 组织和细胞系中检测到上调的 miR-17-5p 和下调的 TIMP2，与它们的正常对应物形成对比。然后，miR-17-5p的过表达显着增加了CC细胞的活力和集落形成能力。此外，Transwell 分析显示 miR-17-5p 促进了侵袭和迁移能力。同时，MMP2和MMP9的表达水平受到抑制miR-17-5p的抑制。荧光素酶分析表明 TIMP2 是 miR-17-5p 的靶标。此外，通过沉默 miR-17-5p 可以抑制 HCC94 细胞中的细胞增殖、侵袭和迁移，而 TIMP2 敲低可以逆转这种情况。总之，所有结果表明miR-17-5p靶向TIMP2通过MMPs信号通路调节CC细胞的增殖、侵袭和迁移；并且 miR-17-5p/TIMP2/MMPs 信号通路有可能成为 CC 的临床治疗靶点。