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. 2021 Jun 16;11:12626. doi: 10.1038/s41598-021-92147-6

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© The Author(s) 2021

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 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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The role of AK5 in the AMPK/mTOR signal pathway in CRC cells. AK5 protein expression, phosphorylated AMPK, and mTOR phosphorylation levels were investigated using immunoblot analysis in three paired CRC tissues and adjacent normal tissues. (a) AK5 and AMPK phosphorylation decreased in CRC tissues compared to adjacent normal tissues. However, phosphorylated mTOR increased in CRC. AK5 protein expression, phosphorylated AMPK, and mTOR phosphorylation were investigated using immunoblot analysis in CRC cell lines after treatment with 5-aza for 1–3 days. (b) 5-aza increased AK5 expression in a time-dependent manner in SW480 and LoVo cells. AMPK phosphorylation increased for 2 days before decreasing 3 days after 5-aza treatment. Phosphorylated mTOR was decreased by 5-aza in both CRC cells. (c) AMPK phosphorylation decreased and mTOR phosphorylation increased when AK5 expression was inhibited by AK5 siRNA transfection into DLD-1 and HCT116 cells for 2 days. (d) AK5 overexpression induced AMPK phosphorylation and decreased phosphorylated mTOR in HT-29 and DLD-1 cell lines after transfection with the overexpression vector for 2 days. The blue arrow shows AK5-GFP, and the red arrow shows only AK5. (e) The migration of HT-29 cells was significantly reduced after 48 h in AK5 overexpression cells transfected with pEGFP-AK5 compared to pEGFP transfected cells. (f) The invasion of DLD-1 cells was significantly reduced after 24 h in AK5 overexpressing cells transfected with pEGFP-AK5 compared to pEGFP transfected cells. (g) The invasion of HCT116 cells was significantly increased after 24 h in AK5 knockdown cells transfected with AK5 siRNA compared to scramble siRNA transfected cells. Full-length bolts images or original gel images of AK5 protein expression are presented in Figure S5a, S5c, S5d, S5e and S5f. Original magnification: × 200. GAPDH or ACTB was used as loading controls. IB immunoblot, AN adjacent normal, T colorectal cancer, 5-aza 5-aza-2′-deoxycytidine. *P-values of < 0.05 were considered statistically significant.