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. 2021 Jan 28;27:7. doi: 10.1186/s10020-020-00261-4

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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/.

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Fig. 6 — MTCH2 knockdown increases temozolomide-induced apoptosis of glioma cells. a, b Images (a) and quantifications (b) of Hoechst staining showing that MTCH2 knockdown promotes cell apoptosis of A172 cells after temozolomide treatment (200 μM, 48 h) (N = 3). Scale bar, 20 μm. c, d Images (c) and quantifications (d) of flow cytometry showing that MTCH2 knockdown promotes apoptosis of A172 cells after temozolomide treatment (200 μM, 48 h) (N = 3). e, f Western blots (e) and quantifications (f) showing that MTCH2 knockdown alters cellular signalings relative to cell survival/death (N = 4)