Exploring chromone-2-carboxamide derivatives for triple-negative breast cancer targeting EGFR, FGFR3, and VEGF pathways: Design, synthesis, and preclinical insights

Drug Dev Res. 2024 Aug;85(5):e22228. doi: 10.1002/ddr.22228.

Abstract

Chromone-based compounds have established cytotoxic, antiproliferative, antimetastatic, and antiangiogenic effects on various cancer cell types via modulating different molecular targets. Herein, 17 novel chromone-2-carboxamide derivatives were synthesized and evaluated for their in vitro anticancer activity against 15 human cancer cell lines. Among the tested cell lines, MDA-MB-231, the triple-negative breast cancer cell line, was found to be the most sensitive, where the N-(2-furylmethylene) (15) and the α-methylated N-benzyl (17) derivatives demonstrated the highest growth inhibition with GI50 values of 14.8 and 17.1 μM, respectively. In vitro mechanistic studies confirmed the significant roles of compounds 15 and 17 in the induction of apoptosis and suppression of EGFR, FGFR3, and VEGF protein levels in MDA-MB-231 cancer cells. Moreover, compound 15 exerted cell cycle arrest at both the G0-G1 and G2-M phases. The in vivo efficacy of compound 15 as an antitumor agent was further investigated in female mice bearing Solid Ehrlich Carcinoma. Notably, administration of compound 15 resulted in a marked decrease in both tumor weight and volume, accompanied by improvements in biochemical, hematological, histological, and immunohistochemical parameters that verified the repression of both angiogenesis and inflammation as additional Anticancer mechanisms. Moreover, the binding interactions of compounds 15 and 17 within the binding sites of all three target receptors (EGFR, FGFR3, and VEGF) were clearly illustrated using molecular docking.

Keywords: EGFR; FGFR3; VEGF; anticancer agents; chromone; triple‐negative breast cancer.

MeSH terms

  • Animals
  • Antineoplastic Agents* / chemical synthesis
  • Antineoplastic Agents* / chemistry
  • Antineoplastic Agents* / pharmacology
  • Apoptosis / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Chromones* / chemical synthesis
  • Chromones* / chemistry
  • Chromones* / pharmacology
  • Chromones* / therapeutic use
  • Drug Design
  • ErbB Receptors* / antagonists & inhibitors
  • ErbB Receptors* / metabolism
  • Female
  • Humans
  • Mice
  • Molecular Docking Simulation*
  • Receptor, Fibroblast Growth Factor, Type 3* / antagonists & inhibitors
  • Receptor, Fibroblast Growth Factor, Type 3* / metabolism
  • Triple Negative Breast Neoplasms* / drug therapy
  • Triple Negative Breast Neoplasms* / metabolism
  • Triple Negative Breast Neoplasms* / pathology
  • Vascular Endothelial Growth Factor A* / metabolism

Substances

  • ErbB Receptors
  • Vascular Endothelial Growth Factor A
  • Antineoplastic Agents
  • Receptor, Fibroblast Growth Factor, Type 3
  • EGFR protein, human
  • Chromones
  • FGFR3 protein, human
  • VEGFA protein, human