Zhou Siyun, Li Yan, Sun Wenqing, Ma Dongyu, Liu Yi, Cheng Demin, Li Guanru, Ni Chunhui
Department of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
Biomedical Publications Center, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
J Biomed Res. 2024 Mar 26;38(2):163-174. doi: 10.7555/JBR.37.20220249.
Epithelial-mesenchymal transition (EMT) is a vital pathological feature of silica-induced pulmonary fibrosis. However, whether circRNA is involved in the process remains unclear. The present study aimed to investigate the role of in the silica-induced EMT and the underlying mechanisms. We found that an elevated expression of promoted EMT and enhanced the migratory capacity of silica-treated epithelial cells. The isolation of cytoplasmic and nuclear separation assay showed that was predominantly expressed in the cytoplasm. RNA immunoprecipitation assay and RNA pull-down experiment indicated that cytoplasmic-localized was capable of binding to miR-497-5p. Furthermore, we found that miR-497-5p attenuated the silica-induced EMT process by targeting transcription factor 3 (TCF3), an E-cadherin transcriptional repressor, in the silica-treated epithelial cells. Collectively, these results reveal a novel role of the /miR-497-5p/TCF3 axis in the silica-induced EMT process in lung epithelial cells. Once validated, this finding may provide a potential theoretical basis for the development of interventions and treatments for pulmonary fibrosis.
上皮-间质转化（EMT）是二氧化硅诱导的肺纤维化的一个重要病理特征。然而，环状RNA是否参与这一过程仍不清楚。本研究旨在探讨[环状RNA名称]在二氧化硅诱导的EMT中的作用及其潜在机制。我们发现[环状RNA名称]表达升高促进了EMT，并增强了二氧化硅处理的上皮细胞的迁移能力。细胞质分离和细胞核分离实验表明，[环状RNA名称]主要在细胞质中表达。RNA免疫沉淀实验和RNA下拉实验表明，定位于细胞质的[环状RNA名称]能够与miR-497-5p结合。此外，我们发现miR-497-5p通过靶向转录因子3（TCF3，一种E-钙黏蛋白转录抑制因子）减弱了二氧化硅处理的上皮细胞中的二氧化硅诱导的EMT过程。总的来说，这些结果揭示了[环状RNA名称]/miR-497-5p/TCF3轴在肺上皮细胞二氧化硅诱导的EMT过程中的新作用。一旦得到验证，这一发现可能为肺纤维化的干预和治疗开发提供潜在的理论基础。
