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. 2018 Nov 22;8:548. doi: 10.3389/fonc.2018.00548

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Copyright © 2018 Li, Li, Shen and Fu.

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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High protein levels of MAPK15 regulate the radiosensitivity in CNE2-IR cells. (A) Western blotting validation on protein levels of five protein kinases (MAPK15, FYN, IKBKB, MAP2K6, and CDK4) in CNE2 and CNE2-IR cells. β-actin served as a loading control. (B) MAPK15 protein expression was significantly reduced in CNE2-IR cells transduced with shMAPK15 lentivirus (sh4). (C) Knockdown of MAPK15 increased radiosensitivity in CNE2-IR cells. The cell viability in NT or shMAPK15 without ionizing irradiation was regarded as 100%, respectively. shMAPK15 (6 Gy) vs. NT (6 Gy), n = 3 *P < 0.05. (D) Knockdown of MAPK15 attenuated colony formation after irradiation in CNE2-IR cells. The colony formation in NT or shMAPK15 without ionizing irradiation was regarded as 100%, respectively. shMAPK15 (6 Gy) vs. NT (6 Gy), n = 3, *P < 0.05. (E) Knockdown of MAPK15 impaired the proliferative potential of CNE2-IR cells exposed to irradiation. The BrdU incorporation in NT without ionizing irradiation was regarded as 100%. shMAPK15 (6 Gy) vs. NT (6 Gy), n = 4, *P < 0.05. (F) Knockdown of MAPK15 increased caspase-3 activity following irradiation in CNE2-IR cells. The caspase-3 activity in NT or shMAPK15 without ionizing irradiation was regarded as 100%, respectively. shMAPK15 (6 Gy) vs. NT (6 Gy), n = 4, *P < 0.05.