Middle East Journal of Cancer (Apr 2022)

Fagonia Arabica Extract Exerts Antitumor Effect on Mice Bearing Ehrlich Carcinoma

  • Sanaa El-Benhawy,
  • Salama EL-Darier,
  • Samia Ebeid,
  • Samar Elblehi,
  • Sabbah Hammoury,
  • Mai El-Sheikh

DOI
https://doi.org/10.30476/mejc.2021.86945.1377
Journal volume & issue
Vol. 13, no. 2
pp. 324 – 336

Abstract

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Background: To date, no studies have investigated the anticancer potential of Fagonia arabica. we aimed to investigate the antitumor potentiality and radiosensitizing effect of Fagonia arabica ethanolic extract (FAEE) on mice bearing solid ehrlich carcinoma (EC). Method: This experimental animal study included 80 Balb-c mice and divided them into four groups: Group I: 10 EC-bearing mice as untreated controls; Group II: 10 EC-bearing mice exposed to a single dose of ionizing radiation (IR) at tumor localization (6Gy); Group III: 30 EC-bearing mice, each 10 mice received different dose of FAEE (250, 500, and 1000 mg/kg/day); Group IV: 30 EC-bearing mice, each 10 mice received different dose of FAEE (250, 500, and 1000 mg/kg/day) plus a single dose of IR (6Gy). P-FOXO3a and p-AKT levels were measured in tumor tissue homogenate via ELISA technique. BCL-2 gene expression was assessed with realtime polymerase chain reaction. Tumor tissues were stained with haematoxylin and eosin stain and examined. Results: FAEE has antiproliferative effect on EC-bearing mice reflected by the decrease in tumor volume and tumor growth rate in a dose-dependent manner. Combination of FAEE with IR significantly increased radiation-induced tumor damage in comparison with IR alone. We observed a significant decrease in the concentration of p-AKT and p-FOXO3a and down-regulation of BCL-2 gene in the EC-bearing mice treated with FAEE only or in combination with IR. Conclusion: FAEE may be an effective antitumor agent against breast cancer. FAEE exerts radio-sensitizing effect, especially at a dose of 500 mg/kg. FAEE interferes with the apoptosis process via decreasing p-AKT and p-FOXO3a and down-regulation of BCL-2 gene.

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