Background: Amygdalin has anticancer benefits because of its active component, hydrocyanic
acid. However, the underlying molecular mechanism is unclear.
Objective: This study aimed to investigate the molecular mechanism by which amygdalin exerts antiproliferative
effects in the human Michigan Cancer Foundation-7 (MCF-7) breast cancer cell line.
Methods: MCF-7 cells were exposed to amygdalin at a particular IC50 value for 24 and 48 hours and
compared to non-treated cells. An Affymetrix whole-transcript expression array was used to analyze
the expression of 32 genes related to DNA replication.
Results: Among the 32 genes, amygdalin downregulated the expression of 16 genes and 19 genes by
>1.5-fold at 24 and 48 hours, respectively. At 24 hours, the downregulated genes from the DNA polymerase
α-primase complex were POLA1, POLA2, PRIM1, and PRIM2; DNA polymerase δ complex:
POLD3; DNA polymerase ε complex: POLE4, Minichromosome Maintenance protein (MCM) complex
(helicase): MCM2, MCM3, MCM4, MCM6, and MCM7; clamp and clamp loader: PCNA; nuclease:
FEN1; and DNA ligase: LIG1. At 48 hours, the downregulated genes from the DNA polymerase
α-primase complex were POLA1, POLA2, and PRIM1; DNA polymerase δ complex: POLD3; DNA
polymerase ε complex: POLE and POLE2; MCM complex (helicase): MCM2, MCM3, MCM4,
MCM5, MCM6, and MCM7; clamp and clamp loader: PCNA, RFC2, and RFC3; RNase H:
RNASEH2A; nucleases: DNA2 and FEN1; and DNA ligase: LIG1.
Conclusion: Amygdalin treatment caused downregulation of several genes that play critical roles in
DNA replication in the MCF-7 cell line. Thus, it might be useful as an anticancer agent.