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. 2022 Nov 2;23:946. doi: 10.1186/s12891-022-05853-1

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© The Author(s) 2022

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. 5 — PKM2 inhibition can reduce the cell apoptosis induced by ATF4 silence under the nutritional deficiency condition

(A) The NP cell proliferation status detected by CCK8 induced by ATF4 silence or PKM2 inhibition under the nutritional deficiency condition (B) The cell apoptosis status detected by flow cytometry under the condition of nutritional deficiency and ATF4 silence or PKM2 inhibition (C) The quantity data showed percentage of cells in apoptosis as showed in B. Data are mean ± s.d. The percentage calculation in each tissue were measured at least 1000 cells each sample. Statistical significance was determined by one-way ANOVA and Student’s t-test. **, ##, △△ P < .001