Gum arabic suppresses proliferation and induces mitochondrial-mediated apoptosis in MCF-7 breast cancer cells via the Bcl-2/Bax/Caspase-9/Caspase-3/7 signaling pathway


Evyapan G., Özdem B.

Journal of Experimental and Clinical Medicine (Turkey), cilt.42, sa.3, ss.314-318, 2025 (Scopus) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 42 Sayı: 3
  • Basım Tarihi: 2025
  • Doi Numarası: 10.52142/omujecm.42.3.14
  • Dergi Adı: Journal of Experimental and Clinical Medicine (Turkey)
  • Derginin Tarandığı İndeksler: Scopus, Academic Search Premier
  • Sayfa Sayıları: ss.314-318
  • Anahtar Kelimeler: apoptosis, breast cancer, caspase, gum Arabic
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

Breast cancer is the most frequently diagnosed cancer among women worldwide, and despite advances in treatment modalities, there remains a critical need for more effective therapeutic strategies. This study investigated the impact of Gum Arabic (GA) on the proliferation and apoptosis of MCF-7 breast cancer cells. The impact of Gum Arabic on cellular viability was assessed using an MTS assay, while its effect on long-term proliferative potential was evaluated via a colony formation assay. To determine the mode of cell death, caspase-3/7 activity assays and Annexin V-FITC/propidium iodide staining were employed. Since MCF-7 cells lack functional caspase-3, the observed caspase-3/7 activity is likely attributable to caspase-7. Additionally, Western blotting was conducted to analyze changes in the expression of key apoptotic proteins. The results revealed that treatment with Gum Arabic led to a dose-dependent reduction in both cell viability and colony formation ability. Moreover, apoptosis was significantly induced in the treated cells. At the molecular level, Gum Arabic administration resulted in a pronounced downregulation of the anti-apoptotic protein B-cell lymphoma 2, along with upregulation of the pro-apoptotic proteins Bcl-2-associated X and caspase-9. These findings demonstrate that Gum Arabic not only suppresses proliferation but also promotes programmed cell death in breast cancer cells through modulation of intrinsic apoptotic pathways. While the results provide preliminary evidence of anticancer potential, further studies in additional breast cancer models, as well as in vivo and clinical investigations, are required before any translational or therapeutic conclusions can be drawn.