Abstract
MicroRNA-24 (miR-24) has been identified to be related to the development of glioma. However, the exact molecular mechanism of miR-24 in glioma progression remains vague. The aim of the present study was to investigate the role of miR-24 in sepsis and to reveal the associated mechanisms. Quantitative real-time polymerase chain reaction was used to compare the levels of miR-24 in glioma and normal tissue. The miR-24 inhibitor or miR-24 mimic was transfected into glioma cells, and then the effects of miR-24 on cell proliferation and apoptosis were detected using CCK-8 (Cell Counting Kit-8) assay and flow cytometry, respectively. Western blot was used to examine the levels of CDX1 (caudal-type homeobox 1), PI3K, p-PI3K, Akt, p-Akt, Cyclin D1, p27, proliferating cell nuclear antigen, Bcl-2, Bax, and Cleaved-casp3. Luciferase assay was used to identify the target gene of miR-24. An animal model was established in mice to detect the role of miR-24 in vivo. These results suggested that miR-24 was elevated in glioma, and miR-24 could promote glioma progression by facilitating cell proliferation and inducing cell apoptosis through CDX1/PI3K/Akt signaling pathway, indicating a novel pathway underlying progression in glioma cells and providing a potential target for glioma treatment.