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. 2020 May 5;5:59. doi: 10.1038/s41392-020-0155-5

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© The Author(s) 2020

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. 6 — Mitochondrial Ca²⁺ promotes dephosphorylation of TFAM to enhance the mitochondrial biogenesis. a Western blotting analysis to measure protein expression levels of MCU, TFAM, and phosphorylated TFAM in LS174 cells, treated as indicated. b Correlation between relative TFAM expression and relative MCU expression in CRC tissue. c Western blotting analysis to measure protein expression levels of MCU, TFAM, and phosphorylated TFAM in LS174 cells, treated as indicated. TFAM S55A, mutation of serine-55 to alanine. Band intensity were quantified by densitometry and represented as the fold change of corresponding control value. d Reverse transcription-quantitative PCR analysis of relative mitochondrial DNA copy number in LS174T cells, treated as indicated. e, f Relative mitochondrial content and mitochondrial ATP levels were determined as mentioned above in LS174T cells treated as indicated. *P < 0.05; **P < 0.01. MCU mitochondrial calcium uniporter, CRC colorectal cancer, TFAM transcription factor A, mitochondrial, Ca²⁺, calcium