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.
Keywords: Cervical cancer; EMT; miR-24; miRNAs.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.