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. 2018 Jan 4;8:960. doi: 10.3389/fphar.2017.00960

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Copyright © 2018 Dai, Yan, Xu, Zeng, Qian, Huo, Li, Sun and Gong.

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) or licensor 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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Akt/GSK3β/β-catenin signaling promotes SCD1-induced TMZ resistance. (A,B) T98G and U87 cells treated with pcDNA-SCD1, EGF or pcDNA-SCD1 plus EGF subjected to MTS assays. (C,D) Cell viability assays were performed after treating T98G-R and U87-R cells with anSCD1 inhibitor (A939572), Akt inhibitors (MK2206 and LY294002) or a combination of A939572 and Akt inhibitors. (E,F) Wound healing assay images captured after treating T98G-R and U87-R cells with A939572, MK2206, LY294002 or a combination of A939572 and Akt inhibitors for 0, 24, and 48 h. Experiments were repeated three times with similar results. ^∗p < 0.05, ^∗∗p < 0.01, ^∗∗∗p < 0.001.