Yağmur DİLBER, Gülçin EKİZÇELI, Elgin Türköz ULUER, Kemal ÖZBİLGİN, Sevinç İNAN
European Journal of Therapeutics - 2026;32(4):388-399
Objective: Lung cancer is characterized by uncontrolled proliferation, loss of apoptosis, angiogenesis, and metastatic potential. Caffeic acid phenethyl ester (CAPE), the major bioactive molecule of propolis, and epigallocatechin gallate (EGCG), a essential polyphenol of green tea, have documented antioxidant, anti-proliferative, and anti-angiogenic effects. This study aimed to investigate the effects of EGCG and CAPE on VEGF and the PI3K/Akt/mTOR signaling pathway, key regulators of lung cancer progression, using in silico and in vitro models. Methods: This study Lung cancer cells (DSMZ/ACC-234) was conducted to demonstrate the inhibition of cell proliferation by the MTT method, molecular binding via autodock vina and protein expression by immunohistochemistry analysis, targeting the VEGF and PI3K/Akt/mTOR pathways with CAPE and EGCG treatment. Results: EGCG and CAPE treatments significantly reduced cell proliferation in lung cancer cells. Untreated cells exhibited strong to very strong immunoreactivity for VEGF and PI3K/Akt/mTOR pathway markers, whereas EGCG reduced these signals to mild-moderate levels and to CAPE moderate-strong levels. Since both treatments resulted in a statistically significant increase in mTORC1 immunoreactivity, molecular docking targeting was performed via it. Conclusion: EGCG and CAPE exhibit significant anti-proliferative and anti-angiogenic effects by adjusting the VEGF and PI3K/Akt/mTOR signaling pathways in lung cancer cells. mTORC1 activation molecular binding affinity is higher in the CAPE-treated group compared to the EGCG group. These findings highlight the therapeutic importance of targeting these pathways in developing novel treatment strategies for lung cancer.
