Inhibition of miR-32 activity promoted EMT induced by PM2.5 exposure through the modulation of the Smad1-mediated signaling pathways in lung cancer cells

- PM2.5 could induce epithelial-to-mesenchymal transition (EMT) in A549 cells and H292 cells.
- Smad1 was up-regulated and I-Smads (Smad6 and Smad7) were down-regulated in the EMT process induced by PM2.5.
- miR-32 was up-regulated in the EMT process induced by PM2.5.
- Knockdown Smad1 can inhibit the EMT process induced by PM2.5.
- Knockdown miR-32 can improve the activation of Smad1 and the EMT process, but reduced the levels of I-Smads.

Epithelial mesenchymal transition (EMT) is a crucial morphological event during tumor progression. The present study reported that EMT could be triggered by airborne fine particulate matter (PM) with a mean diameter of less than 2.5 μm (PM2.5) in human lung cancer cells. We also aimed to elucidate the possible mechanisms of these processes. The results showed that treatment with PM2.5 promoted the activity of the SMAD family member 1 (Smad1)-mediated signaling pathway and downregulated the expression of the inhibitory Smad proteins Smad6 and Smad7 in lung cancer cells. Moreover, the knockdown of Smad1 suppressed the EMT process induced by PM2.5 exposure. Our data further revealed that miR-32 has a negative effect on PM2.5-induced EMT. The results showed that the expression level of miR-32 was significantly upregulated in the PM2.5-induced EMT process. The knockdown of miR-32 enhances the activity of the Smad1-mediated signaling pathway, which promotes the EMT process induced by PM2.5. Thus, these findings indicate that PM2.5 can induce the EMT process through the Smad1-mediated signaling pathway, and miR-32 may act as an EMT inhibitor in lung cancer cells.

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