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. 2020 May 29;15:55. doi: 10.1186/s13020-020-00338-6

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — The “multi-points priming” mechanisms of NCTD on inhibiting proliferation and inducing apoptosis. NCTD: norcantharidin; PI3K: phosphoinositide 3 kinase; NF-κB: nuclear factor-kappa B; MAPK: mitogen-activated protein kinase; JNK: Jun N-terminal kinase; PP1: protein phosphatase type 1; PP2A: protein phosphatase 2A; PP2B: protein phosphatase 2B; Cdc6: cell division cycle protein 6; CD1: cyclin D1; CDKs: cyclin-dependent kinases; CDKIs: cyclin-dependent kinase inhibitors; Bcl-2: B-cell lymphoma-2; (−): Inhibition; (+): Promotion or inducing