Akademik Veri Yönetim Sistemi
49th FEBS Congress,, İstanbul, Türkiye, 5 - 09 Temmuz 2025, ss.13, (Özet Bildiri)
Lung adenocarcinoma (LUAD), the most common subtype of non-small cell lung cancer, makes up 40% of all lung cancers. In recent years, in addition to standard chemotherapeutic agents in treatment, research has focused on targeted therapies and combined treatment options that can increase the effects of existing treatments and reduce their side effects. Eribulin mesylate (EM) is a synthetic analog of halichondrin B, derived from marine sponges, and acts as a tubulin-binding agent that suppresses microtubules through a mechanism different from taxanes. Curcumin, a natural compound, is one of the most potent chemopreventive and anti-cancer agents. Diphenyl-difluoroketone (EF24) is one of the synthetic analogs of curcumin and has better pharmacological properties than curcumin. A549 cells were treated with different concentrations of EF24 (0.5–32 lM) or EM (5–100 nM) alone or in combination for 24 and 48 h. MTT and lactate dehydrogenase (LDH) assays were performed to determine cell viability and cytotoxicity, respectively. The enzyme levels of DFFB [caspase-acti-vated DNase (CAD)] were evaluated by ELISA. The active caspase-8 protein levels were detected by western blot, and beta-actin protein was used for normalization. Compared to control cells, significant reductions in cell viability were observed at EF24 concentrations of 4 lM and above and all EM concentrations at 24 and 48 hours. The rate of LDH release was 9% in EF24, 15% in 10 nM EM, and 1% in EF24 + EM. Compared with single-agent treatments, the decrease in combined administration was statistically significant (p < 0.05). It was determined that there were no statistically significant changes in DFFB levels. Additionally, EF24 was found to increase active caspase-8 levels by 1.08, EM by 1.46, and EF24 + EM by 2.13 times compared to the control cells. Statistical significance was determined by the student’s t-test. Our results have shown that EF24 enhances the effect of the extrinsic apoptotic response induced by EM.