Correction: J ExpClin Cancer Res 41, 322 (2022)
https://doi.org/10.1186/s13046-022-02532-w
Following the publication of the original article [1], one of the readers spotted an error in the supplementary materials. The Supplementary figures of Additional file 1 is missing and the e-files for Additional file 1 and Additional file 2 were interchanged.
The correction does not have any effect on the results or conclusions of the paper. The original article has been corrected.
Reference
Zhao R, He B, Bie Q, et al. AQP5 complements LGR5 to determine the fates of gastric cancer stem cells through regulating ULK1 ubiquitination. J Exp Clin Cancer Res. 2022;41:322. https://doi.org/10.1186/s13046-022-02532-w.
Author information
Authors and Affiliations
Corresponding authors
Supplementary Information
Additional file1: Figure S1.
Expression of marker genes in gastric cancer tissue epithelial/stem cells and cultured adherent/spheroid cells. Figure S2. AQP5 expression in AGS/HGC-27/GES-1 spheroids and adherent cells. Figure S3. AQP5 promotes gastric cancer development in vitro and in vivo. Figure S4. Expression of AQP5 in GC-CSCs. Figure S5. AQP5 promotes the stemness of GC-CSCs. Figure S6. Effect of AQP5 on LGR5 expression. Figure S7. Cellular pathways affected by AQP5. Figure S8. ATG7 is the key regulator of GC cell autophagy. Figure S9. AQP5 affects key autophagy proteins. Figure S10. AQP5 promotes malignant behaviors of GC-CSCs by regulating K63-mediated ubiquitination of ULK1. Figure S11. Interaction of AQP5, TRIM21 and ULK1. Figure S12. AQP5 promotes self-renewal via TRIM21 in GC-CSCs.
Additional file 2: Supplementary Table 1.
Sequences of real-time PCR primers. Supplementary Table 2. Primary Antibodies. Supplementary Table 3. Second Antibodies. Supplementary Table 4. ShRNA or siRNA Oligonucleotides. Supplementary Table 5. Tumorigenicity of knockdown AQP5 and control group. Supplementary Table 6. Tumorigenicity of knockdown AQP5 and control group. Supplementary Table 7. Tumorigenicity of knockdown AQP5 and LGR5. Supplementary Table 8. Differentially expressed genes between exogenous overexpression of AQP5 and control group. Supplementary Table 9. Differentially expressed genes between exogenous overexpression of AQP5 and control group. Supplementary Table 10. Identification of the AQP5 protein complex by mass spectrometry.
Rights and permissions
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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
About this article
Cite this article
Zhao, R., He, B., Bie, Q. et al. Correction: AQP5 complements LGR5 to determine the fates of gastric cancer stem cells through regulating ULK1 ubiquitination. J Exp Clin Cancer Res 41, 342 (2022). https://doi.org/10.1186/s13046-022-02557-1
Published:
DOI: https://doi.org/10.1186/s13046-022-02557-1