Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the impact and mechanism of doxycycline on TGF beta one induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells.
Western blot and immunofluorescence staining were used to determine the expression levels, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cell migration ability.
Doxycycline (0-10 μg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. In contrast, E-cadherin expression was upregulated in TGF beta one induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited TGF beta one induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells.
The study concluded that Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.