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Sci Rep ; 13(1): 11346, 2023 07 13.
Artículo en Inglés | MEDLINE | ID: mdl-37443185

RESUMEN

In the current study, we designed and synthesized a series of new quinoline derivatives 10a-p as antiproliferative agents targeting cancer through inhibition of VEGFR-2. Preliminary molecular docking to assess the interactions of the designed derivatives with the binding site of VEGFR-2 (PDB code: 4ASD) displayed binding poses and interactions comparable to sorafenib. The synthesized compounds exhibited VEGFR-2 inhibitory activity with IC50 ranging from 36 nM to 2.23 µM compared to sorafenib (IC50 = 45 nM), where derivative 10i was the most potent. Additionally, the synthesized derivatives were evaluated in vitro for their cytotoxic activity against HepG2 cancer cell line. Seven compounds 10a, 10c, 10d, 10e, 10i, 10n and 10o (IC50 = 4.60, 4.14, 1.07, 0.88, 1.60, 2.88 and 2.76 µM respectively) displayed better antiproliferative activity than sorafenib (IC50 = 8.38 µM). Compound 10i was tested against Transformed Human Liver Epithelial-2 normal cell line (THLE-2) to evaluate its selective cytotoxicity. Furthermore, 10i, as a potent representative of the series, was assayed for its apoptotic activity and cell cycle kinetics' influence on HepG2, its effects on the gene expression of VEGFR-2, and protein expression of the apoptotic markers Caspase-7 and Bax. Compound 10i proved to have a potential role in apoptosis by causing significant increase in the early and late apoptotic quartiles, a remarkable activity in elevating the relative protein expression of Bax and Caspase-7 and a significant reduction of VEGFR-2 gene expression. Collectively, the obtained results indicate that compound 10i has a promising potential as a lead compound for the development of new anticancer agents.


Asunto(s)
Antineoplásicos , Quinolonas , Humanos , Estructura Molecular , Relación Estructura-Actividad , Caspasa 7/metabolismo , Sorafenib/farmacología , Quinolonas/farmacología , Receptor 2 de Factores de Crecimiento Endotelial Vascular/metabolismo , Simulación del Acoplamiento Molecular , Proteína X Asociada a bcl-2 , Inhibidores de Proteínas Quinasas/farmacología , Ensayos de Selección de Medicamentos Antitumorales , Antineoplásicos/química , Proliferación Celular , Diseño de Fármacos
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