Abstract
Nanoparticles of neodymium oxide (NPs-Nd2O3) can induce respiratory-related diseases, including lung tissue injury when entering the organism through the respiratory tract. However, it is currently unclear whether they can induce epithelial-mesenchymal transition (EMT) in lung tissue and the related mechanisms. In this study, we investigated the function of circ_009773 in the process of EMT induced by NPs-Nd2O3 in lung tissue from in vivo as well as in vitro experiments. The findings showed that NPs-Nd2O3 induced EMT in 16HBE cells and SD rat lung tissues. This was characterised by a decrease in epithelial markers and an increase in mesenchymal markers. Additionally, circ_009773 expression was found to decrease in 16HBE cells infected with NPs-Nd2O3 and also decreased in the lung tissues of SD rats. Relevant experiments showed that circ_009773 inhibited EMT in NPs-Nd2O3-treated 16HBE cells and SD rat lung tissues. The previous experiments revealed that circ_009773 was localised in the cytoplasm and functioned at the post-transcriptional level. With the EMT-related pathway used as the basis for circ_009773-related competing endogenous (ce)RNA mechanisms, our observations indicate that circ_009773 is capable of binding to and regulating the expression of miR-135b-5p. In summary, we found that circ_009773 inhibits the EMT induced by NPs-Nd2O3 in lung tissues, and this process likely occurs through competitive binding to miR-135b-5p.