C Zhao1, X-B Wang, Y-H Zhang, Y-M Zhou, Q Yin, W-C Yao. 1. Department of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao, China. xia6555916142@163.com.
Abstract
OBJECTIVE: To investigate the expressions, biological effects and potential mechanism of miR-424 in glioma. METHODS AND METHODS: A total of 54 glioma tissues and 12 normal brain tissues were collected. Human glioma cells (A172, SHG-44, T98, LN18, and LN229) and normal human astrocytes (NHAs) were cultured. Cell invasion and migration capacities were detected by transwell assay. KIF23 was predicted and confirmed as a direct target of miR-424 by TargetScan prediction and Dual-luciferase reporter assay. Six-week-old female nude mice were used for Xenograft tumor formation assay. RESULTS: Results of this study demonstrated a significant decrease of miR-424 expressions both in glioma cells and tissues. Moreover, the declined miR-424 expressions were observed to be correlated with the poor OS and worse clinicopathological parameters of glioma patients. Functional assays indicated that miR-424 restoration could inhibit the glioma cell epithelial-to-mesenchymal transition (EMT) and metastasis, as well as the tumor growth rate and tumor size of glioma mice. Additionally, kinesin family member 23 (KIF23) expressions were found to be significantly enhanced in glioma specimens, and KIF23 was considered to be a functional target for miR-424 in glioma. CONCLUSIONS: MiR-424, considered as a tumor-suppressor, inhibited cell metastasis and EMT by targeting KIF23 in glioma, which may provide a novel insight into tumorigenesis and the basis for the development of miRNA-targeting therapies against glioma.
OBJECTIVE: To investigate the expressions, biological effects and potential mechanism of miR-424 in glioma. METHODS AND METHODS: A total of 54 glioma tissues and 12 normal brain tissues were collected. Humanglioma cells (A172, SHG-44, T98, LN18, and LN229) and normal human astrocytes (NHAs) were cultured. Cell invasion and migration capacities were detected by transwell assay. KIF23 was predicted and confirmed as a direct target of miR-424 by TargetScan prediction and Dual-luciferase reporter assay. Six-week-old female nude mice were used for Xenograft tumor formation assay. RESULTS: Results of this study demonstrated a significant decrease of miR-424 expressions both in glioma cells and tissues. Moreover, the declined miR-424 expressions were observed to be correlated with the poor OS and worse clinicopathological parameters of gliomapatients. Functional assays indicated that miR-424 restoration could inhibit the glioma cell epithelial-to-mesenchymal transition (EMT) and metastasis, as well as the tumor growth rate and tumor size of gliomamice. Additionally, kinesin family member 23 (KIF23) expressions were found to be significantly enhanced in glioma specimens, and KIF23 was considered to be a functional target for miR-424 in glioma. CONCLUSIONS:MiR-424, considered as a tumor-suppressor, inhibited cell metastasis and EMT by targeting KIF23 in glioma, which may provide a novel insight into tumorigenesis and the basis for the development of miRNA-targeting therapies against glioma.