DNA-PKcs/AKT1 inhibits epithelial-mesenchymal transition during radiation-induced pulmonary fibrosis by inducing ubiquitination and degradation of Twist1

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作者信息关键词期刊信息基础信息归属信息摘要

成果类型：

期刊论文

作者：

Yan, Ziyan;Zhu, Jiaojiao;Liu, Yuhao;Li, Zhongqiu;Liang, Xinxin;...

通讯作者：

Zhou, Ping-Kun;Gu, YQ

作者机构：

[Zhou, Ping-Kun; Gu, Yongqing; Wang, Ping; Huang, Xin; Zhu, Jiaojiao; Zhou, Lin; Yan, Ziyan; Gu, YQ; Liu, Yuhao; Gao, Shanshan] Beijing Inst Radiat Med, Beijing Key Lab Radiobiol, Beijing 100850, Peoples R China.

[Li, Zhongqiu] Chinese Acad Sci, Inst Zool, State Key Lab Stem Cell & Reprod Biol, Beijing, Peoples R China.

[Chen, Huixi; Gu, Yongqing; Liang, Xinxin; Zhou, Shenghui; Ao, Xingkun] Univ South China, Hengyang Med Coll, Hengyang, Peoples R China.

[Hou, Yifan; Gu, Yongqing] Hebei Univ, Coll Life Sci, Baoding, Peoples R China.

通讯机构：

[Zhou, PK; Gu, YQ ] B

Beijing Inst Radiat Med, Beijing Key Lab Radiobiol, Beijing 100850, Peoples R China.

语种：

英文

关键词：

DNA-PKcs;epithelial–mesenchymal transition;radiation-induced pulmonary fibrosis;Twist1;VND3207

期刊：

Clinical and Translational Medicine

ISSN：

2001-1326

年：

2024

卷：

期：

页码：

e1690-

DOI：

10.1002/ctm2.1690

基金类别：

National Natural Science Foundation of China; [82073488]; [82273568]; [81773359]; [32171238]; [82230108]; [31470827]

机构署名：

本校为其他机构

摘要：

IntroductionRadiation-induced pulmonary fibrosis (RIPF) is a chronic, progressive, irreversible lung interstitial disease that develops after radiotherapy. Although several previous studies have focused on the mechanism of epithelial-mesenchymal transition (EMT) in lung epithelial cells, the essential factors involved in this process remain poorly understood. The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) exhibits strong repair capacity when cells undergo radiation-induced damage; whether DNA-PKcs regulates EMT during RIPF remains unclear.ObjectivesTo investigate the role and mo...

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DNA-PKcs/AKT1 inhibits epithelial-mesenchymal transition during radiation-induced pulmonary fibrosis by inducing ubiquitination and degradation of Twist1

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