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. 2017 Sep 11;18(9):1945. doi: 10.3390/ijms18091945

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Inhibition of the Akt-mTOR pathway and activation of the JNK pathway are implicated in SH-mediated autophagy. (A) SH dose-dependently suppressed the Akt-mTOR pathway and activated the JNK pathway in U87 and SF767 cells, along with the induction of autophagy. The cells were treated with different concentrations of SH for 24 h; (B) Effects of IGF-1 on SH-mediated autophagy and suppression of the Akt-mTOR pathway in U87 and SF767 cells. The cells were treated with SH (0.5 mM) for 24 h in the absence or presence of IGF-1; (C) Effects of SP600125 on SH-mediated autophagy and the JNK pathway activation in U87 and SF767 cells. The cells were treated with SH (0.5 mM) for 24 h in the absence or presence of SP600125. β-actin served as the loading control. All blots shown are representative of n = 3 experiments, with similar results.

Inhibition of the Akt-mTOR pathway and activation of the JNK pathway are implicated in SH-mediated autophagy. (A) SH dose-dependently suppressed the Akt-mTOR pathway and activated the JNK pathway in U87 and SF767 cells, along with the induction of autophagy. The cells were treated with different concentrations of SH for 24 h; (B) Effects of IGF-1 on SH-mediated autophagy and suppression of the Akt-mTOR pathway in U87 and SF767 cells. The cells were treated with SH (0.5 mM) for 24 h in the absence or presence of IGF-1; (C) Effects of SP600125 on SH-mediated autophagy and the JNK pathway activation in U87 and SF767 cells. The cells were treated with SH (0.5 mM) for 24 h in the absence or presence of SP600125. β-actin served as the loading control. All blots shown are representative of n = 3 experiments, with similar results.