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. 2021 Sep 23;21:509. doi: 10.1186/s12935-021-02212-3

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© The Author(s) 2021

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. 7 — MDK acts via PI3K-Akt signaling to influence GBM cell proliferation, migration, and invasion. Western blot analysis of p-Akt, Akt, p-ERK, ERK, p-PI3K, PI3K and β-actin in GBM cell lines T98G and U87-MG in which MDK was knocked down (KD), and in GBM cell lines A172 and U251-MG in which MDK was overexpressed (OE). Negative control (NC) cells were also analyzed in parallel. MDK: midkine; GBM: glioblastoma; IB: immunoblotting