宫颈癌（CC）是妇科最常见的恶性肿瘤。尽管进行常规手术，晚期宫颈癌很难完全切除。微小RNA-24（miR-24）在多种肿瘤中发挥调控作用，但其在宫颈癌中的调控功能以前未知。我们在宫颈癌细胞中建立了稳定的miR-24和磷酸酶和张力蛋白同源物（PTEN）的敲低模型。我们用RT-PCR和西方印迹法测量mRNA和蛋白表达。我们使用CCK8、Transwell、划痕愈合和流式细胞术分别评估细胞增殖、侵袭、迁移和凋亡。我们还在裸鼠转移瘤模型中检查miR-24和PTEN对肿瘤生长的影响。miR-24的表达在CC组织和细胞系（C-33A，HeLa S3，SiHa）中显著增加。miR-24抑制剂极大地抑制了PTEN/PI3K/AKT的活性，而miR-24模拟剂明显激活了这个信号通路。PTEN的敲低显著逆转了miR-24抑制剂对宫颈癌细胞增殖、侵袭、迁移和凋亡的影响。由miR-24抑制剂引起的肿瘤生长抑制作用和ki67表达的显著逆转效应，被si-PTEN逆转。miR-24抑制剂明显抑制了细胞增殖、侵袭、迁移、上皮间质转化（EMT）过程和肿瘤生长，同时促进细胞凋亡。然而，si-PTEN明显逆转了miR-24抑制剂的影响。定位miR-24可能为预防和治疗宫颈癌提供了一种新的治疗策略。© 2023. 作者以授予Springer Science+Business Media, LLC, 的独家许可。Springer Nature的一部分。

Cervical cancer (CC) is the most prevalent malignant tumor in gynecology. Despite routine surgery, advanced CC is hard to remove completely. MicroRNA-24 (miR-24) regulates several types of tumors, but its regulatory function in CC was previously unknown. We established stable knockdown of miR-24 and phosphatase and tensin homolog (PTEN) in CC cells. We measured mRNA and protein expression with RT-PCR and western blotting. We evaluated cell proliferation, invasion, migration, and apoptosis with CCK8, Transwell, wound healing, and flow cytometry, respectively. We also examined the influence of miR-24 and PTEN on tumor growth in a metastatic tumor model in nude mice. The expression of miR-24 was significantly increased in CC tissues and cell lines (C-33A, HeLa S3, SiHa). MiR-24 inhibitor greatly suppressed PTEN/PI3K/AKT, while miR-24 mimic markedly activated this signaling pathway. Knockdown of PTEN significantly reversed the effects of miR-24 inhibitor on cell proliferation, invasion, migration, and apoptosis of CC cells. The significant inhibition effect of tumor growth and ki67 expression caused by miR-24 inhibitor was reversed by si-PTEN. MiR-24 inhibitor significantly suppressed cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT) process, and tumor growth, while promoting cell apoptosis. However, the influence of miR-24 inhibitor was markedly reversed by si-PTEN. Targeting miR-24 could provide a novel therapeutic strategy for the prevention and treatment of CC.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.