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. 2022 Jun 3;13(6):523. doi: 10.1038/s41419-022-04980-w

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© The Author(s) 2022

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

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Fig. 7 — a Dot plot of the KEGG enrichment pathways in the SGLT2 inhibitor treatment group. b Heatmap of the SGLT2 inhibitor treatment-related genes that participated in the PI3K-AKT pathway in MNNG/HOS cells. c Western blot analysis of the protein expression levels of AKT and p-AKT in MG-63 and MNNG/HOS cell lines treated with canagliflozin (1 uM) for 24 h. GAPDH served as an internal reference. RT-PCR analysis (d) and Western blot analysis (e) of the mRNA and protein expression levels in MG-63 and MNNG/HOS cell lines treated with canagliflozin (1 uM), MK2206 (10 μM), or the combination of canagliflozin (1 uM) and MK2206 (10 μM). Data are presented as the mean ± SD of three independent experiments (ns not significant; ***p < 0.001). RT-PCR analysis (f) and Western blot analysis (g) of the mRNA and protein expression levels of specific genes in MG-63 and MNNG/HOS cell lines treated with canagliflozin (1 uM), SC-79 (20 μM), or the combination of canagliflozin (1 uM) and SC-79 (20 μM) for 24 h. Data are presented as the mean ± SD of three independent experiments (ns not significant; ***p < 0.001).