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

Xin Wen; Si Chen; Xueting Chen; Hui Qiu; Wei Wang; Nie Zhang; Wanming Liu; Tingting Wang; Xin Ding; Longzhen Zhang

doi:10.3389/fonc.2022.887068

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

Front Oncol. 2022 Sep 30:12:887068. doi: 10.3389/fonc.2022.887068. eCollection 2022.

Authors

Xin Wen^{1

2}, Si Chen^{1

3}, Xueting Chen¹, Hui Qiu¹, Wei Wang¹, Nie Zhang¹, Wanming Liu¹, Tingting Wang¹, Xin Ding¹, Longzhen Zhang^{1

2

4}

Affiliations

¹ Department of Radiation Oncology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
² Cancer Institute of Xuzhou Medical University, Xuzhou, China.
³ Department of Radiation Oncology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
⁴ Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou, China.

Abstract

Pancreatic adenocarcinoma (PAAD) is one of the most aggressive digestive system tumors in the world, with a low early diagnosis rate and a high mortality. Integrin beta 5 (ITGB5) is demonstrated to be a potent tumor promoter in several carcinomas. However, it is unknown whether ITGB5 participates in the occurrence and development of PAAD. In this study, we confirmed a high expression of ITGB5 in PAAD and its role in promoting invasiveness and transitivity in PAAD. Besides, the knockdown of ITGB5 increased cell sensitivity to radiation by promoting DNA damage repair and the MEK/ERK signaling pathway. Collectively, these results show that ITGB5 plays an essential role in pancreatic cancer growth and survival.

Keywords: DNA damage repair; ITGB5; MEK/ERK signaling pathway; pancreatic adenocarcinoma (PAAD); radio-sensitivity.