- Correction
- Open Access
- Published:
Correction to: ALG3 contributes to stemness and radioresistance through regulating glycosylation of TGF-β receptor II in breast cancer
Journal of Experimental & Clinical Cancer Research volume 41, Article number: 117 (2022)
Correction to: J Exp Clin Cancer Res 40, 149 (2021)
https://doi.org/10.1186/s13046-021-01932-8
Following publication of the original article [1], the authors identified minor errors in Fig. 5, specifically:
The corrected figure is given here. The corrections do not have any effect on the final conclusions of the paper. The original article has been corrected.
ALG3 enhances radioresistance via regulation of TGFBR2 glycosylation. a Downshift of TGFBR2 bands in ALG3-sg cells was detected by Western blot. But not TGFBR1 bands (b) Representative immunofluorescence images of TGFBR2 expression level in cytoplasmic and membrane fractions. c A schematic model of different subtypes of N-glycans. The round spots are mannose, the square ones are acetylglucosamine, and the red spot is the initial of the N-glycosylation site, which is initiated by ALG3. d TGFBR2 band shift could be seen in ALG3-sg cells or cells treated by tunicamycin. And downregulation of ALG3 reduced the expression level of p-SMAD2. e Representative immunofluorescence images of p-SMAD2 expression level in cytoplasmic and nuclear fractions. Nuclear translocation of p-SMAD2 was significantly decreased in ALG3-sg and tunicamycin treatment groups. f The co-immunoprecipitation between TGFBR1 and TGFBR2, TGFBR1 and p-SMAD2 could be detected in ALG3-control group, but not tunicamycin treatment, and ALG3-sg groups. g TGFBR2 inhibitor (LY2109761) in ALG3-transduced cells decreased the surviving fraction of breast cancer cells after radiation treatment, which were detected by CCK-8 assays. Data were analyzed by two-way ANOVA. Each bar represents the mean ± SD of three independent experiments. h Inhibition of TGFBR2 in ALG3-transduced cells decreased the number of colonies after radiation treatment. i Inhibition of TGFBR2 in ALG3-transduced cells decreased the proportion of CD44+CD24− cells, which were detected by flow cytometry. “ns” no significance, *P < 0.05
Reference
Sun X, He Z, Guo L, et al. ALG3 contributes to stemness and radioresistance through regulating glycosylation of TGF-β receptor II in breast cancer. J Exp Clin Cancer Res. 2021;40:149. https://doi.org/10.1186/s13046-021-01932-8.
Author information
Authors and Affiliations
Corresponding authors
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
Sun, X., He, Z., Guo, L. et al. Correction to: ALG3 contributes to stemness and radioresistance through regulating glycosylation of TGF-β receptor II in breast cancer. J Exp Clin Cancer Res 41, 117 (2022). https://doi.org/10.1186/s13046-022-02322-4
Published:
DOI: https://doi.org/10.1186/s13046-022-02322-4