LncRNA MALAT1, an lncRNA acting via the miR-204/ZEB1 pathway, mediates the EMT induced by organic extract of PM2.5 in lung bronchial epithelial cells

Extensive cohort studies have explored the hazards of particulate matter with aerodynamic diameter 2.5 mu m or smaller (PM2.5) to human respiratory health; however, the molecular mechanisms for PM2.5 carcinogenesis are poorly understood. Long non-coding RNAs (incRNAs) are involved in various pathophysiological processes. In the present study, we investigated the effect of PM2.5 on the epithelial-mesenchymal transition (EMT) in lung bronchial epithelial cells and the underlying mechanisms mediated by an lncRNA. Organic extracts of PM2.5 from Shanghai were used to treat human bronchial epithelial cell lines (HBE and BEAS-2B). The PM2.5 organic extracts induced the EMT and cell transformation. High levels of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), mediated by NF-kappa B. were involved in the EMT process. For both cell lines, there was a similar response. In addition, MALAT1 interacted with miR-204 and reversed the inhibitory effect of its target gene, ZEB1, thereby contributing to the EMT and malignant transformation. In sum, these findings show that NF-kappa B transcriptionally regulates MALAT1, which, by binding with miR-204 and releasing ZEB1, promotes the EMT. These results offer an understanding of the regulatory network of the PM2.5-induced EMT that relates to the health risks associated with PM2.5.