Investigation of the Effect of Triacetyl Resveratrol on Epithelial-Mesenchymal Transition in Human Lung Cancer Cell...

Our study aimed to investigate the effects of Triacetyl resveratrol (TCRV) on epithelial-mesenchymal transition (EMT) in human lung cancer cell lines. Different concentrations of TCRV were applied to the A549 cell line for 24 and 48 h. The IC50 value of TCRV was determined by cell viability with the CCK-8 test. Expression levels of E-cadherin and vimentin were analysed by immunocytochemistry and qPCR after incubation with TCRV at the determined dose. Apoptosis was assessed by acridine orange/ethidium bromide (AO/EB) staining, and possible interactions of TCRV with target proteins were evaluated by in silico molecular docking. Morphological changes were observed in A549 cells application with the IC50 dose of TCRV, showing decreased cell integrity and altered morphology compared to controls. While E-cadherin and vimentin levels decreased in 24-h application, an increase in both markers was observed in 48-h application. It was determined by the AO/EBr staining method that TCRV significantly increased apoptosis and, according to the in silico molecular docking results, TCRV showed a strong binding tendency with E-cadherin and vimentin. It was demonstrated that TCRV exhibits time-dependent antiproliferative, apoptotic and EMT-regulating effects in A549 cells. While significant anti-proliferative and cytotoxic effects were observed in short-term applications, cellular restructuring and EMT-like processes were triggered along with resistance development in some cells in long-term applications; however, increased stress and apoptosis were determined in the general cell population. Molecular modelling results indicate that TCRV exhibits a strong binding affinity for E-cadherin (-7.00 kcal/mol) and vimentin (-7.70 kcal/mol) at the structural level; however, while these binding data reflect the possibility of direct protein interactions, it should not be overlooked that TCRV may play an active role in the regulation of indirect regulatory mechanisms, such as transcriptional changes.