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. 2020 Apr 8;26:28. doi: 10.1186/s10020-020-00152-8

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — NEAT1 and Akt signaling downregulation were involved in the shikonin against paclitaxel-resistant NSCLC. a Either low dose or high dose of shikonin considerably suppressed the NEAT1 knockdown A549/PTX cell growth. b Either low dose or high dose of shikonin considerably induced the cell apoptotic death in NEAT1 knockdown A549/PTX cells. c p-Akt expression was decreased, cleaved PARP and cleaved caspase-3 expression were increased after shikonin treatment in NEAT1 knockdown A549/PTX cells. d The proliferation of NEAT1 overexpression A549/PTX cells was not inhibited after shikonin treatment. e Apoptosis rates were not enhanced after shikonin treatment. f Shikonin could not decrease p-Akt expression, also could not increase cleaved PARP and cleaved caspase-3 expression after shikonin treatment in NEAT1 knockdown A549/PTX cells. *Statistically significant difference (p < 0.05). #No statistically significant difference(p > 0.05)