Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM
- Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of (China)
- Graduate College of Hebei Medical University, Shijiazhuang, People’s Republic of (China)
Highlights: • The expression level of ZMYND11 in GBM tumor tissue and U87 cell line. • The role of ZMYND11 upregulation in U87 cells in vitro and vivo. • The link of expression level between ZMYND11 and miR-196a-5p in GBM tumor and U87 cells. ZMYND11 (zinc finger MYND-type containing 11) has been widely regarded to be involved in a variety of cancers as a potential suppressor. However, the biological role and mechanism of ZMYND11 in glioblastoma multiform (GBM) remain unknown. In this study, we found that ZMYND11 expression was remarkably decreased in GBM tissues from 20 cases and cell line (U87) compared to normal brain tissue from 10 cases (P < 0.001). Furthermore, we explored that ZMYND11 upregulation significantly suppressed U87 cells proliferation and invasion, induced cell cycle arrest and apoptosis in vitro. Subsequently, we identified increased ZMYND11 inhibited the tumor growth using tumor cells xenograft experiment on rude mice. Moreover, we explored that ZMYND11 was a new direct and functional target of miR-196a-5p in U87 via luciferase reporter assay. In addition, we confirmed the negative correlation between miR-196a-5p and ZMYND11 in GBM tissue and U87 cells by changing the expression level of miR-196a-5p with lentivirus and plasmid vector. Furthermore, we demonstrated that decreased ZMYND11 could reverse suppressive effect of downregulated miR-196a-5p on U87 by rescue experiment. Taken together, ZMYND11 was demonstrated to be a potential and extremely promising suppressor of GBM, while miRNA-196a-5p was quite an important target of treatment of GBM.
- OSTI ID:
- 22897548
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 494, Issue 3-4; Other Information: Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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