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Abstract
Correction: J Exp Clin Cancer Res 39, 144 (2020) https://doi.org/10.1186/s13046-020-01646-3 Following the publication of the original article [1], the authors identified errors in the images of Fig. 3, Fig. 5, Fig. 8, Fig. 10 and Supplementary Material Table S4, specifically: * Fig.3D - incorrect image for Eca109 with IFI6-KD * Fig.5G - incorrect fluorescence data for TE-1 cells * Fig.8A - incorrect fluorescence image for Eca109 * Fig.8G - incorrect band of GAPDH for TE-1 cells * Fig.10C - incorrect representative image for IFI6 staining in the OEControl and IFI6-OE groups were included * Table S4 - Incorrect primer sequences for MCU, ATF3 and NCLX were uploaded The corrected figures are provided below: Fig.3D - incorrect image for Eca109 with IFI6-KD Fig.5G - incorrect fluorescence data for TE-1 cells Fig.8A - incorrect fluorescence image for Eca109 Fig.8G - incorrect band of GAPDH for TE-1 cells Fig.10C - incorrect representative image for IFI6 staining in the OEControl and IFI6-OE groups were included Table S4 - Incorrect primer sequences for MCU, ATF3 and NCLX were uploaded The corrected figures are provided below: Statistical significance was determined by one-way ANOVA. **P < 0.01 Full size image Correct Figure 3 Fig. 3 figure 2 IFI6 promotes cell proliferation, inhibits apoptosis and ameliorates oxidative stress in ESCC. a-b. Statistical significance was determined by one-way ANOVA. **P < 0.01. i. The indicated ESCC cells were incubated in the presence or absence of the MCU inhibitor DS16570511 (10 μM), and mitochondrial ROS levels were then measured by MitoSOX staining, followed by flow cytometry Full size image Correct Figure 5 Fig. 5 figure 4 IFI6 modulates mitochondrial ROS production by regulating mitochondrial Ca2+ overload. a-b.
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