MicroRNA‐195‐5p/E2F7 Axis Underlies the Antimicrobial Additive Triclosan‐Induced Cytotoxicity in Human Pulmonary Epithelial Cells

Due to its widespread applications over a few decades, triclosan (TCS), a broad-spectrum biocide, is commonly found in different environmental matrices and organisms, including human body fluids and tissues. In addition, chronic exposure to TCS could contribute to adverse health effects in humans. Hence, the current study was undertaken to investigate the cytotoxic effects of TCS and the underlying molecular mechanism. TCS exposure in pulmonary epithelial cells, including human normal bronchial as well as adenocarcinoma alveolar basal cells, caused decreased cell viability, higher levels of reactive oxygen species production, mitochondrial dysfunction, arrest in cell cycle progression, and apoptosis, which was associated with an elevated microRNA-195-5p (miR-195-5p) expression. Moreover, inhibition of miR-195-5p attenuated TCS-induced cytotoxic effects. Target prediction algorithms identified that E2F transcription factor 7 (E2F7) may be a direct target of miR-195-5p. Furthermore, transfection of miR-195-5p mimic markedly inhibited E2F7 gene expression. Finally, ectopic overexpression of E2F7 effectively suppressed TCS-mediated cytotoxic effects. Thus, TCS induces cytotoxic effects via the miR-195-5p/E2F7 axis.