Department of Gynecology Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, No. 758 Fuma Road, Fuzhou, 350014, China.
Biochem Genet. 2024 Apr;62(2):1277-1290. doi: 10.1007/s10528-023-10491-w. Epub 2023 Aug 17.
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.
宫颈癌（CC）是妇科最常见的恶性肿瘤。尽管常规手术，但晚期 CC 很难完全切除。MicroRNA-24（miR-24）调节多种类型的肿瘤，但它在 CC 中的调节功能尚不清楚。我们在 CC 细胞中建立了 miR-24 和磷酸酶和张力蛋白同源物（PTEN）的稳定敲低。我们使用 RT-PCR 和 Western blot 测量 mRNA 和蛋白质表达。我们分别使用 CCK8、Transwell、划痕愈合和流式细胞术评估细胞增殖、侵袭、迁移和细胞凋亡。我们还在裸鼠转移瘤模型中检查了 miR-24 和 PTEN 对肿瘤生长的影响。miR-24 在 CC 组织和细胞系（C-33A、HeLa S3、SiHa）中的表达显著增加。miR-24 抑制剂显著抑制了 PTEN/PI3K/AKT，而 miR-24 模拟物则显著激活了该信号通路。PTEN 敲低显著逆转了 miR-24 抑制剂对 CC 细胞增殖、侵袭、迁移和凋亡的影响。miR-24 抑制剂对肿瘤生长和 ki67 表达的显著抑制作用被 si-PTEN 逆转。miR-24 抑制剂显著抑制细胞增殖、侵袭、迁移、上皮-间充质转化（EMT）过程和肿瘤生长，同时促进细胞凋亡。然而，miR-24 抑制剂的影响被 si-PTEN 明显逆转。靶向 miR-24 可能为 CC 的预防和治疗提供新的治疗策略。
