This article is a correction to:
ITGB5 promotes innate radiation resistance in pancreatic adenocarcinoma by promoting DNA damage repair and the MEK/ERK signaling pathway
Xin Wen1,2†
Si Chen1,3†
Xueting Chen1†
Hui Qiu1Wei Wang1
Nie Zhang1
Wanming Liu1
Tingting Wang1
Xin Ding1*
Longzhen Zhang1,2,4*- 1Department of Radiation Oncology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
- 2Cancer Institute of Xuzhou Medical University, Xuzhou, China
- 3Department of Radiation Oncology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
- 4Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou, China
A Corrigendum on
ITGB5 promotes innate radiation resistance in pancreatic adenocarcinoma by promoting DNA damage repair and the MEK/ERK signaling pathway
by Wen X, Chen S, Chen X, Qiu H, Wang W, Zhang N, Liu W, Wang T, Ding X and Zhang L (2022) Front. Oncol. 12:887068. doi: 10.3389/fonc.2022.887068
Error in Figure/Table
In the published article, there was an error in Figure 5 and Figure 7 as published. Due to our careless work, we took multiple images of each group at the same time and saved all the images in the same folder. In Figure 5, images in pCDH were taken following taking images in sg-ITGB5, so that two images are confused partly. Similar mistake happened in Figure 7.]. The corrected [Figure 5 and Figure 7] and its caption [Figure 5 The effect of ITGB5 expression on migration and invasion on pancreatic cancer cells. **p<0.01, ***p<0.001] and [Figure 7 The effect of ITGB5 expression on radiation sensitization in pancreatic cancer cells. (A, C) The colony formation of PANC-1 (A) and BXPC3 (C) cells irradiated with different doses; (B, E) Plating efficiency (PE) of PANC-1 (B) and BXPC3 (E) cells; (C, F) Survival fraction (SF) of PANC-1 (C) and BXPC3 (F) cells; (G-H) Survival fraction curves of PANC-1 (G) and BXPC3 (H) cells according to Linear-quadratic model and Single-hit multitarget model. Values were presented as mean ± SD (n=3).] appear below.
Figure 5
Figure 5 The effect of ITGB5 expression on migration and invasion on pancreatic cancer cells. **p<0.01, ***p<0.001.
Figure 7
Figure 7 The effect of ITGB5 expression on radiation sensitization inpancreatic cancer cells. (A, C) The colony formation of PANC-1 (A) and BXPC3 (C) cells irradiated with different doses; (B, E) Plating efficiency (PE) of PANC-1 (B) and BXPC3 (E) cells; (C, F) Survival fraction (SF) of PANC-1 (C) and BXPC3 (F) cells; (G-H) Survival fraction curves of PANC-1 (G) and BXPC3 (H) cells according to Linear-quadratic model and Single-hit multitarget model. Values were presented as mean ± SD (n=3).
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: pancreatic adenocarcinoma (PAAD), ITGB5, radio-sensitivity, MEK/ERK signaling pathway, DNA damage repair
Citation: Wen X, Chen S, Chen X, Qiu H, Wang W, Zhang N, Liu W, Wang T, Ding X and Zhang L (2024) Corrigendum: ITGB5 promotes innate radiation resistance in pancreatic adenocarcinoma by promoting DNA damage repair and the MEK/ERK signaling pathway. Front. Oncol. 14:1381151. doi: 10.3389/fonc.2024.1381151
Received: 02 February 2024; Accepted: 07 February 2024;
Published: 22 February 2024.
Edited and Reviewed by:
Sumitra Deb, Virginia Commonwealth University, United StatesCopyright © 2024 Wen, Chen, Chen, Qiu, Wang, Zhang, Liu, Wang, Ding and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Xin Ding, ZGluZ3hpbjgxQDE2My5jb20=; Longzhen Zhang, anN4eWZ5emx6QDEyNi5jb20=
†These authors have contributed equally to this work