H-Z Shi1, D-N Wang, L-N Ma, H Zhu. 1. Department of Neurosurgery, Yantaishan Hospital, Yantai, Shandong Province, P.R. China. zhuhe1983@hust.edu.cn.
Abstract
OBJECTIVE: Glioblastoma (GBM) is a deadly brain cancer that seriously threatens the lives of patients. Moreover, various microRNAs (miRNAs) have been found to be involved in the progression of GBM. The purpose of this study is to preliminarily elucidate the regulatory mechanism of miR-362 in GBM. PATIENTS AND METHODS: The abnormal expression of miR-362 and MAPK1 was detected by RT-qPCR or Western blot analysis in GBM tissues and cells. CCK-8 and transwell assays were performed to measure cell proliferation, migration and invasion. The relationship between miR-362 and MAPK1 was confirmed by luciferase reporter assay. RESULTS: MiR-362 expression was reduced in GBM tissues and cells. The decreased expression of miR-362 predicted poor prognosis in GBM patients. Functionally, overexpression of miR-362 inhibited the proliferation and metastasis of GBM cells. In addition, miR-362 directly targets MAPK1. MAPK1 was negatively correlated with miR-362 expression in GBM. Moreover, MAPK1 was upregulated and served as a tumor promoter in GBM. More importantly, the upregulation of MAPK1 weakened the inhibitory effect of miR-362 on cell proliferation and metastasis in GBM. CONCLUSIONS: MiR-362 restrains cell proliferation and metastasis in GBM by targeting MAPK1, indicating that miR-362 functions as a tumor suppressor in GBM.
OBJECTIVE:Glioblastoma (GBM) is a deadly brain cancer that seriously threatens the lives of patients. Moreover, various microRNAs (miRNAs) have been found to be involved in the progression of GBM. The purpose of this study is to preliminarily elucidate the regulatory mechanism of miR-362 in GBM. PATIENTS AND METHODS: The abnormal expression of miR-362 and MAPK1 was detected by RT-qPCR or Western blot analysis in GBM tissues and cells. CCK-8 and transwell assays were performed to measure cell proliferation, migration and invasion. The relationship between miR-362 and MAPK1 was confirmed by luciferase reporter assay. RESULTS:MiR-362 expression was reduced in GBM tissues and cells. The decreased expression of miR-362 predicted poor prognosis in GBM patients. Functionally, overexpression of miR-362 inhibited the proliferation and metastasis of GBM cells. In addition, miR-362 directly targets MAPK1. MAPK1 was negatively correlated with miR-362 expression in GBM. Moreover, MAPK1 was upregulated and served as a tumor promoter in GBM. More importantly, the upregulation of MAPK1 weakened the inhibitory effect of miR-362 on cell proliferation and metastasis in GBM. CONCLUSIONS:MiR-362 restrains cell proliferation and metastasis in GBM by targeting MAPK1, indicating that miR-362 functions as a tumor suppressor in GBM.