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. 2020 Jul 31;10:1166. doi: 10.3389/fonc.2020.01166

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Copyright © 2020 He, Li, Rong, Gao, Mu, Guan, Ren, Zi, Liu, Fan, Zhou, Duan, Zhou, Deng and Sun.

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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IGF1R is a key downstream gene of YTHDC2. (A) Fifty-six genes related to the PI3K-AKT/S6 signaling pathway were found to be upregulated in the GSE48501 dataset, among which IGF1R is the key downstream target gene of YTHDC2 by using m6A prediction database (m6avar.renlab.org) (B) PI3K-AKT signaling was activated in radiation-resistance NPC cells. (C) Western blot analyses of PI3K-AKT/S6 signaling activation in radiation resistant cells. (D) A positive correlation between the expressions of YTHDC2 and IGF1R in NPC tissues was found by analyzing GSE102349 dataset. (E) Knockdown of YTHDC2 in CNE2-IRR cells downregulated IGF1R protein expression and inactivated PI3K-AKT/S6 signaling. (F) Overexpression of YTHDC2 in CNE2 and HK1 cells upregulated IGF1R protein expression and activated PI3k-AKT signaling. All experiments were repeated twice.