Zhiming Ma1. 1. Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, PR China. Electronic address: mazhimingabc@163.com.
Abstract
BACKGROUND: SETD8 (named PR-SET7 or KMT5a) has been reported to regulate various biological processes including carcinogenesis. However, the role of SETD8 in glioma progression has not been investigated. METHOD: qPCR and western blot were used to detect the expression levels of miR-382 and SETD8. MTT and wound healing assay used to detect the cell proliferation and migratory capability. A predicted target of miR-382 (SETD8) was first validated using a luciferase assay. RESULTS: In this study, we found that SETD8 expression was evidently upregulated in glioma tissues and glioma cells, compared with the adjacent normal tissues and normal human astrocytes (NHA). Next, we showed that SETD8 evidently induced cell proliferation and migration in vitro and in vivo. In addition,dual-luciferase assays revealed that miR-382 directly regulates oncogenic SETD8 expression in U87 and U251 cells. Finally a statistically significant inverse correlation of miR-382 and SETD8 expression was observed in 30 glioma patients. CONCLUSION: These data indicated that oncogenic SETD8 was regulated by miR-382 and involved glioma progression, revealing new therapeutic targets for glioma cancer.
BACKGROUND:SETD8 (named PR-SET7 or KMT5a) has been reported to regulate various biological processes including carcinogenesis. However, the role of SETD8 in glioma progression has not been investigated. METHOD: qPCR and western blot were used to detect the expression levels of miR-382 and SETD8. MTT and wound healing assay used to detect the cell proliferation and migratory capability. A predicted target of miR-382 (SETD8) was first validated using a luciferase assay. RESULTS: In this study, we found that SETD8 expression was evidently upregulated in glioma tissues and glioma cells, compared with the adjacent normal tissues and normal human astrocytes (NHA). Next, we showed that SETD8 evidently induced cell proliferation and migration in vitro and in vivo. In addition,dual-luciferase assays revealed that miR-382 directly regulates oncogenic SETD8 expression in U87 and U251 cells. Finally a statistically significant inverse correlation of miR-382 and SETD8 expression was observed in 30 gliomapatients. CONCLUSION: These data indicated that oncogenic SETD8 was regulated by miR-382 and involved glioma progression, revealing new therapeutic targets for glioma cancer.