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. 2020 Dec 15;7:582097. doi: 10.3389/fmed.2020.582097

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Copyright © 2020 Zhang, Chen, Deng, Long, Xu and Liu.

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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Hsa-miR-106a inhibits the expression of RUNX3 and enhances radiation sensitivity. (A) Alignment of the predicted miRNA binding sites in the 3′ untranslated region (UTR) of the RUNX3 mRNA. (B) Luciferase reporter gene demonstrated that hsa-miR-106a directly targeted the 3′ UTR of RUNX3. (C) The protein expression of RUNX3 in FaDu, UM-SCCC-4, UM-SCC47, and UPCI-SCC90. (D) Hsa-miR-106a transfection efficiency was measured by RT-qPCR. (E) The mRNA expression of RUNX3 in human papillomavirus (HPV)-negative cells with hsa-miR-106a overexpression and HPV-positive cells with hsa-miR-106a silencing. (F) The sensitivity of the cells to radiation was detected by clonogenic survival with the condition of hsa-miR-106a overexpression in HPV-negative cells and hsa-miR-106a silencing in HPV-positive cells. *p < 0.05, **p < 0.01, ***p < 0.001.