Transcription factor TP63 mediates LncRNA CNTFR-AS1 to promote DNA damage induced by neodymium oxide nanoparticles via homologous recombination repair

被引：5

作者：

Gao, Lei ^{[1
]}

Zhang, Xia ^{[1
]}

Cui, Jinjin ^{[1
]}

Liu, Ling ^{[1
]}

Tai, Dapeng ^{[1
]}

Wang, Suhua ^{[1
]}

Huang, Lihua ^{[1
]}

机构：

[1] Baotou Med Coll, Sch Publ Hlth, Baotou 014030, Inner Mongolia, Peoples R China

来源：

ENVIRONMENTAL POLLUTION | 2023年 / 334卷

关键词：

Long non-coding RNA CNTFR-AS1; DNA damage; Homologous recombination repair; HALLMARKS; CELLS;

D O I：

10.1016/j.envpol.2023.122191

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

The widespread use of neodymium oxide nanoparticles (NPs-Nd2O3) has caused environmental pollution and human health problems, thus attracting significant attention. Understanding the mechanisms of NPs- Nd2O3- inducedgenetic damage is of great significance for identifying early markers for NPs-Nd2O3-induced lung injury. At present, the mechanisms underlying DNA damage induced by NPs-Nd2O3 remain unclear. In this study, we performed functional assays on human bronchial epithelial cells (16HBEs) exposed to various concentrations of NPs-Nd2O3 and SD rats administered with a single intratracheal instillation with NPs-Nd2O3. Exposure to NPs-Nd2O3 could lead to DNA damage in 16HBE cells and rat lung tissue cells. We found a novel long non-coding RNA, named CNTFR-AS1, which was highly expressed after exposure to NPs-Nd2O3. Our data verified that transcription factor TP63 mediates the high expression levels of CNTFR-AS1, which in turn regulates NPs-Nd2O3- induced DNA damage in cells by inhibiting HR repair. Moreover, the levels of CNTFR-AS1 were correlated with the number of years worked by occupational workers. Collectively, these results demonstrate that CNTFR-AS1 acts as a novel DNA damage regulator in bronchial epithelial cells exposed to NPs-Nd2O3. Hence, our data provide a basis for the identification of lncRNAs as early diagnostic markers for rare earth lung injury.

引用

页数：11