Corrigendum to: Small proline-rich repeat protein 3 enhances the sensitivity of esophageal cancer cells in response to DNA damage-induced apoptosis.

Abstract

Molecular OncologyVolume 16, Issue 14 p. 2766-2767 CorrigendumOpen Access Corrigendum to: Small proline-rich repeat protein 3 enhances the sensitivity of esophageal cancer cells in response to DNA damage-induced apoptosis This article corrects the following: Small proline-rich repeat protein 3 enhances the sensitivity of esophageal cancer cells in response to DNA damage-induced apoptosis Aiping Luo, Hongyan Chen, Fang Ding, Yu Zhang, Mingrong Wang, Zefen Xiao, Zhihua Liu, Volume 7Issue 5Molecular Oncology pages: 955-967 First Published online: June 13, 2013 First published: 20 July 2022 https://doi.org/10.1002/1878-0261.13284AboutSectionsPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat The article by Luo et al. [[1]] contained inadvertent duplications between two western blot images presented in Figs 2B and 5A, and between two western blot images presented in Fig. 5B. The authors have corrected this by providing the original raw data for all experimental replicates, and the revised figures are included here. All authors agree to this corrigendum and confirm that changes do not affect the conclusions of the article. The authors apologize for any inconvenience caused. The corrected figures are reproduced below. Fig. 2. Overexpression of SPRR3 triggered caspase activation in response to DNA damage. A & B) Overexpression of SPRR3 enhances the processing of caspase 3. Cells were exposed to cisplatin (10 mM, A) or X-IR (4 Gy, B) and analyzed after the indicated time by Western blot for the processing of caspase 3. β-actin was probed as a loading control. C) Cells were treated with cisplatin or X-IR as indicated. Caspase 3 activity was measured by luminescent assay. Data shown are Mean ± SD from multiple independent experiments (*P < 0.05). Fig. 5. Overexpression of SPRR3 activates Bax and causes the release of cytochrome c. A) Cells were exposed to cisplatin (10 mM) or X-IR (4 Gy) at the indicated time. Overexpression of SPRR3 increased the expression of Bax and p53 compared with controls. B) Overexpression of SPRR3 caused Bax mitochondria translocation and the release of cytochrome c. Cells were subjected to subcellular fractionation after treatment. The cytosolic (Cyto) and mitochondrial (Mito) fractions were analyzed by Western blot. C) Co-immnunoprecipitation analysis showing that interaction of SPRR3 with Bcl-2 was increased after cisplatin treatment. D & E) Overexpression of SPRR3 abolished the Bcl-2-mediated anti-apoptosis. EC9706 cells were transiently cotransfected with various amounts of HA-SPRR3 with constant amount of GFP-Bcl-2 expression plasmids. After transfection, cells were treated with 10 mM cisplatin for 24 h and harvested. Cells were subjected to subcellular fractionation, and detected by Western blot. Reference 1Luo A, Chen H, Ding F, Zhang Y, Wang M, Xiao Z, et al. Small proline-rich repeat protein 3 enhances the sensitivity of esophageal cancer cells in response to DNA damage-induced apoptosis. Mol Oncol. 2013; 7: 955– 67. https://doi.org/10.1016/j.molonc.2013.05.005Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Volume16, Issue14July 2022Pages 2766-2767 ReferencesRelatedInformation