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. 2021 Jun 23;11:647175. doi: 10.3389/fonc.2021.647175

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Copyright © 2021 Yu, Chan, Lin, Chiou, Lin, Chen, Lee, Chi, Chen, Huang, Chew, Hsu, Yang and Hung

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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The knockdown of IRAK2 promoted resistance to IR-induced apoptosis in OML1 and SCC25 cells. (A) Endogenous IRAK2 expression in different OSCC cell lines, showing higher expressions of IRAK2 in OML1 and SCC25 than that of OML1-R and SCC4 cells. The values under bands represented the relative density that normalized to β-actin. (B) When compared with their control cells, post-irradiation colony formation rates were increased in IRAK2-knockdown OML1 (P = 0.0009) and SCC25 (P = 0.0577) cells. (C) Effect of radiation, IRAK2 shRNA or both on cell apoptosis in OML1 and SCC25 cell lines. Flow cytometry analysis using Annexin V and 7-AAD staining was performed to detect apoptotic cells. (D) IRAK2-shRNA transfection decreased the expressions of cleaved caspase-8 and caspase-3 in OML1 (left) and SCC25 (right) cancer cells. Densitometry-derived values (bottom) were normalized with the control set as 1. β-actin served as the loading control for normalization.