Erdogan, AyseKoras, Rahime Aybike2026-01-242026-01-2420251991-007X1991-0088https://doi.org/10.3329/bjp.v20i1.80949https://hdl.handle.net/20.500.12868/5372The intention of this work was to analyze that carvacrol could enhance cancer-inhibiting potency of cetuximab (monoclonal antibody) in lung cancer cells. The combination of cetuximab and carvacrol was found to co-operatively suppress cell proliferation by enhancing apoptosis and inducing cell cycle arrest in A-549 and H1299 cells. Furthermore, the combination therapy triggered cell death by inducing membrane disruption. The most effective combinations were IC10 cetuximab + IC10 carvacrol for A-549 and IC20 cetuximab + IC10 carvacrol for H1299 (CI = 2.0). LDH activity increased by 101% in A-549 and 239% in H1299 (p<0.05). Caspase-3 activity rose by 1.6-fold in A549 and 1.4-fold in H1299 (p<0.05). The combination decreased PCNA, topoisomerase II-alpha, and cyclins D1, D2, E, A, and B (p<0.05). Overall, the combination of carvacrol and cetuximab appears to enhance anti-cancer efficacy and may significantly improve therapeutic outcomes in lung cancer cells.eninfo:eu-repo/semantics/openAccessGrowth-Factor ReceptorMonoclonal-AntibodyNeck-CancerChemical-CompositionEssential OilsEgfrExpressionAntioxidantChemotherapyInhibitionArticle10.3329/bjp.v20i1.809492012-s2.0-105005893503Q3WOS:001480746800004Q4