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. 2018 Jul 31;8:11470. doi: 10.1038/s41598-018-29929-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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(A) Among T98G and LN18 cells treated for 36 hours with PBS, TMZ (200 μM), NDV (MOI 1) or a combination of TMZ (200 μM) and NDV (MOI 1), the combination-treated cells showed the most obvious signs of apoptosis at the protein level. (B) The AKT/mTOR pathway was markedly inhibited, and AMPK was activated. (C) Similar AKT suppression was also found in the U87, U251 and C6 cell lines. (D) T98G and LN18 cells were treated with TMZ (200 μM), NDV (moi 1), MK2206 (2 μM) or their combination for 42 hours; p-AKT, AKT and β-tubulin were detected by Western blotting. (E,G) Cell viability was detected by MTT assay (*P < 0.05). (F) T98G and LN18 cells were treated with TMZ (200 μM), NDV (MOI 1), compound C (2 μM) or their combination for 42 hours; p-AMPK, AMPK and β-tubulin were detected by Western blotting. (H) T98G and LN18 cells were treated with TMZ (200 μM), AT13148 (5 μM) or their combination for 36 hours; p-AKT, AKT, Parp1, cleaved BID and β-tubulin were detected by Western blotting. (I) Cell viability was detected by MTT assay (*P < 0.05, AT13148 and TMZ vs TMZ alone or AT13148 alone).