Αξιολόγηση της επίδρασης του ψυχρού ατμοσφαιρικού πλάσματος στο πρόγραμμα EMT σε καρκινικά κύτταρα πνεύμονα A549

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for most cases. Tumor progression and metastasis are closely associated with the epithelial-to-mesenchymal transition (EMT) program, a biological process through which epithelial cells acquire mesenchymal characteristics, resulting in enhanced migratory and invasive properties. EMT is also accompanied by alterations in cell-extracellular matrix (ECM) interactions and ECM remodeling, which contribute to tumor cell migration and invasion. Transforming growth factor-beta (TGFβ) is one of the principal inducers of EMT and contributes significantly to cancer progression. In recent years, Cold Atmospheric Plasma (CAP), a partially ionized gas rich in reactive oxygen and nitrogen species, has emerged as a promising anticancer approach due to its selective effects on cancer cells and its ability to modulate multiple cellular pathways. The present study aimed to investigate the effects of CAP on TGFβ-induced EMT in A549 human lung adenocarcinoma cells. EMT was induced by treatment with TGFβ1, while CAP was applied as a pre-treatment before TGFβ stimulation. The effects of CAP on EMT were evaluated through morphological observations, circularity analysis, wound healing assays, immunofluorescence staining for E-cadherin and F-actin, quantitative real-time PCR analysis, and western blot analysis of signaling molecules involved in EMT regulation. TGFβ treatment induced characteristic EMT-associated changes, including alterations in cell morphology, reduced cell circularity, enhanced migratory capacity, downregulation of the epithelial marker E-cadherin, and alterations in the expression of mesenchymal markers and ECM-remodeling markers. CAP pre-treatment partially reversed several of these effects, resulting in increased cellular circularity, reduced migration, and attenuation of EMT-associated molecular alterations. Furthermore, CAP influenced signaling pathways associated with EMT regulation, suggesting that its anti-EMT activity may involve modulation of both canonical and non-canonical TGFβ signaling mechanisms. Overall, the findings of this study demonstrate that CAP can suppress key features of TGFβ-induced EMT in A549 cells and highlight its potential as a novel therapeutic strategy for limiting lung cancer progression and metastasis.