Long non-coding RNA NONHSAT217600.1 is involved in the regulation of neodymium oxide-induced cytotoxicity in 16HBE cells.

Autor: Hong, Jiaru, Xiao, Xietian, Li, Ting, Wang, Huandong, Hua, Qiuhan
Zdroj: Molecular & Cellular Toxicology; Apr2024, Vol. 20 Issue 2, p325-333, 9p
Abstrakt: Background: Neodymium oxide (Nd2O3) is a rare-earth metal oxide with extensive applications in various fields. Long non-coding RNAs(lncRNAs), which are molecules longer than 200 ribonucleotides, have attracted great attention toward their critical roles in modulating the response to cytotoxic agents such as Nd2O3. Objective: This study aimed to explore the cytotoxic effects of Nd2O3 in 16HBE human bronchial epithelial cells, with a focus on the involvement of lncRNAs. Results: Nd2O3 particle exposure increased extracellular lactate dehydrogenase (LDH) release in a dose- and time-dependent manner. Viability assays indicated that Nd2O3 treatment reduced 16HBE cell survival, and comet assays confirmed the DNA-damaging effect of Nd2O3 exposure. Furthermore, Nd2O3 exposure induced an alteration in lncRNA expression profiles, contributing to the upregulation of lncRNA NONHSAT217600.1 in 16HBE cells. Functional experiments indicated that the inhibition of lncRNA NONHSAT217600.1 expression alleviated Nd2O3-induced cytotoxicity, suppressing LDH release, enhancing cell viability, and reducing DNA damage in 16HBE cells. Transcriptome sequencing and bioinformatics analysis suggested that lncRNA NONHSAT217600.1 participates in the regulation of DNA damage-related pathways as well as in other aspects of cellular function in response to Nd2O3. Conclusion: This study demonstrates the regulatory roles of lncRNA NONHSAT217600.1 in Nd2O3-induced cytotoxicity, providing evidence for the potential of lncRNAs in the risk/hazard assessment of rare-earth element-related toxicity. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
Externí odkaz: