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. 2021 Jul 26;11:648152. doi: 10.3389/fonc.2021.648152

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Copyright © 2021 Liu, Li, Wu, Tang, Li and Shi

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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E2F6 is the functional target of the COX10-AS1/miR-641 axis. (A) The putative binding sites of miR-641 on E2F6 were predicted by an online database. (B) The relative expression of E2F6 in clinical specimen. (C) The relative expression of E2F6 in different grade of glioma. (D) The relative expression of E2F6 in primary and recurrent glioma. (E) Pearson’s correlation analysis of COX10-AS1 expression and E2F6 expression in clinical specimens. (F) Pearson’s correlation analysis of miR-641 expression and E2F6 expression in clinical specimens. (G, H) The relative expression of E2F6 in NHAs and glioma cell lines measured by qRT-PCR and western blot. (I) The expression level of E2F6 in different grades of glioma detected by immunohistochemistry. (J, K) Luciferase reporter assay indicated that miR-641 reduced the luciferase activity of E2F6-WT but not E2F6-MUT. (L, M) The relative expression of E2F6 in U87 and LN229 cells transfected with sh-COX10-AS1, miR-641 inhibitor or sh-COX10-AS1 together with miR-641 inhibitor, as measured by qRT-PCR and western blot. **P < 0.01.