AMYGDALIN AS A POTENTIAL THERAPY FOR BREAST CANCER VIA BAX/BCL2 GENE-MEDIATED APOPTOSIS

Abstract

Breast cancer (BC) remains one of the most common and difficult-to-treat malignant diseases in global public health, requiring the development of more selective and less toxic therapeutic approaches. In this context, natural compounds have gained increasing attention due to their biological potential in regulating tumor cell processes. Amygdalin (C20H27NO11), a natural cyanogenic glycoside found in the seeds of plants from the Rosaceae family and often referred to as “vitamin B17”, has been studied for its possible anticancer effects. This study aimed to evaluate the effect of amygdalin on the expression of apoptosis-related genes and on cell viability in two human BC cell lines with different molecular profiles: MDA-MB-231 and MCF-7. The cells were treated with amygdalin at a concentration of 50 mg/mL for 24 hours, while NHDF (Normal Human Dermal Fibroblast) cells (Sigma Aldrich) were used as the control group. The expression levels of the pro-apoptotic gene BAX and the anti apoptotic gene BCL-2 were assessed using RT-qPCR, while cell viability was analyzed using standard cytotoxicity methods. The results showed a cell-specific gene expression modulation. In MDA-MB-231 cells, amygdalin treatment led to an increase in the expression of both BAX and BCL-2 genes. In MCF-7 cells, a decrease in the expression of both genes was observed, together with a significant reduction in cell viability. These findings suggest that amygdalin has different biological effects depending on the cellular context and tumor molecular profile, thus supporting its potential role in modulating apoptotic pathways in BC cells and pointing towards the amygdalin therapeutic applicability.