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整合素β5（ITGB5）通过促进DNA损伤修复和MEK/ERK信号通路，增强胰腺腺癌的固有辐射抗性。

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

作者信息

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

机构信息

Department of Radiation Oncology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

Cancer Institute of Xuzhou Medical University, Xuzhou, China.

出版信息

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

DOI:10.3389/fonc.2022.887068
PMID:36249018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9563233/
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.

摘要

胰腺腺癌（PAAD）是全球侵袭性最强的消化系统肿瘤之一，早期诊断率低，死亡率高。整合素β5（ITGB5）在多种癌症中被证明是一种强大的肿瘤促进因子。然而，ITGB5是否参与PAAD的发生和发展尚不清楚。在本研究中，我们证实了ITGB5在PAAD中的高表达及其在促进PAAD侵袭性和转移性中的作用。此外，敲低ITGB5通过促进DNA损伤修复和MEK/ERK信号通路增加细胞对辐射的敏感性。总体而言，这些结果表明ITGB5在胰腺癌的生长和存活中起着至关重要的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/b7ddf7031a8c/fonc-12-887068-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/8383f64392d7/fonc-12-887068-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/aa80c15936a4/fonc-12-887068-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/b7ddf7031a8c/fonc-12-887068-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/42afd9bea35a/fonc-12-887068-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/b7d5ab6db628/fonc-12-887068-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/feb0e23a929e/fonc-12-887068-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/a6144c861bdc/fonc-12-887068-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/8acb2c29625f/fonc-12-887068-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/bf819ecbd79c/fonc-12-887068-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/b3a7f2cfa194/fonc-12-887068-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/8383f64392d7/fonc-12-887068-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/aa80c15936a4/fonc-12-887068-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df0e/9563233/b7ddf7031a8c/fonc-12-887068-g010.jpg

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