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ITGB5 promotes innate radiation resistance in pancreatic adenocarcinoma by promoting DNA damage repair and the MEK/ERK signaling pathway
Frontiers in Oncology ( IF 3.5 ) Pub Date : 2022-09-30 , DOI: 10.3389/fonc.2022.887068
Xin Wen 1, 2 , Si Chen 1, 3 , Xueting Chen 1 , Hui Qiu 1 , Wei Wang 1 , Nie Zhang 1 , Wanming Liu 1 , Tingting Wang 1 , Xin Ding 1 , Longzhen Zhang 1, 2, 4
Affiliation  

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.



中文翻译:


ITGB5通过促进DNA损伤修复和MEK/ERK信号通路促进胰腺腺癌的先天性辐射抵抗



胰腺癌(PAAD)是世界上最具侵袭性的消化系统肿瘤之一,早期诊断率低,死亡率高。整合素β 5 (ITGB5) 被证明是多种癌症中有效的肿瘤促进剂。但ITGB5是否参与PAAD的发生、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 侵袭性和传递性中的作用。此外,ITGB5的敲低通过促进DNA损伤修复和MEK/ERK信号通路来增加细胞对辐射的敏感性。总的来说,这些结果表明 ITGB5 在胰腺癌的生长和生存中发挥着重要作用。

更新日期:2022-09-30
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