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. 2018 Oct 26;8:15897. doi: 10.1038/s41598-018-34154-8

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© The Author(s) 2018

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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NOX4 is required for mitochondrial function in thyroid cancer during hypoxia. (A,B) Mitochondrial ROS level was measured with MitoSox staining by flow cytometry analysis in TPC-1 cells cultured in 1% O₂ for 48 hours (A). NOX4 transfection can rescue mROS production decreasing after cell was treated with 1% O₂ for 48 hours (B). (C) Mitochondrial membrane potential assessed by TMRE (50 nM) staining of NOX4 knockdown TPC-1 cells. (D) Whole-TPC-1 cell oxygen consumption rate (OCR) in different groups. The dotted lines indicate the time of adding oligomycin (1 μM), FCCP (1 μM) and rotenone and antimycin A (Rot/AA, 1 μM each).