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CORRECTION article

Front. Oncol., 22 February 2024
Sec. Cancer Molecular Targets and Therapeutics

Corrigendum: ITGB5 promotes innate radiation resistance in pancreatic adenocarcinoma by promoting DNA damage repair and the MEK/ERK signaling pathway

  • 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
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Figure 5 The effect of ITGB5 expression on migration and invasion on pancreatic cancer cells. **p<0.01, ***p<0.001.

Figure 7
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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.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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 States

Copyright © 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, dingxin81@163.com; Longzhen Zhang, jsxyfyzlz@126.com

These authors have contributed equally to this work

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.