LncPOPDC3-1 promotes Cd-induced inflammation response in human bronchial epithelial cells via the miR-548a-3p/NF-κB axis.

Cadmium (Cd), a pervasive environmental heavy metal pollutant, has been extensively documented for its toxic effects on human health. However, the underlying pathogenic mechanisms of Cd toxicity, spanning molecular to cellular levels, remain incompletely elucidated and warrant further investigation. Here, quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) analyses demonstrated that cadmium exposure induced a pronounced inflammatory response, characterized by significant elevation of interleukin-6 (IL-6) and interleukin-8 (IL-8) in 16HBE cells. High-throughput sequencing of cadmium-exposed versus control 16HBE cells identified LncPOPDC3-1 as a novel differentially expressed transcript showing marked upregulation during cadmium-triggered inflammation. We found that LncPOPDC3-1 accelerated the progression of inflammation, including increasing inflammatory factors IL-6 and IL-8. Mechanistically, dual luciferase reporter gene assays and qRT-PCR analysis have demonstrated that LncPOPDC3-1 can directly bind to miR-548a-3p, which regulated the activation of NF-κB signaling pathway. Following inhibition of the NF-κB signaling pathway, the regulatory effect of LncPOPDC3-1 on Cd-induced inflammation was significantly attenuated. Therefore, our data suggest that LncPOPDC3-1 regulates the activation of NF-κB pathway through competitive bound to miR-548a-3p, which subsequently promotes the Cd-induced inflammation in 16HBE cells. This provides a new mechanism and potential molecular targets for Cd-induced toxicity.