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.

背景：苦杏仁苷具有抗癌功效，因为它的活性成分是氢氰酸。然而，潜在的分子机制尚不清楚。

目的：本研究旨在探讨苦杏仁苷在人类密歇根癌症基金会-7 (MCF-7) 乳腺癌细胞系中发挥抗增殖作用的分子机制。

方法：将 MCF-7 细胞暴露于特定 IC ₅₀值的苦杏仁苷24 和 48 小时，并与未处理的细胞进行比较。使用 Affymetrix 全转录表达阵列来分析 32 个与 DNA 复制相关的基因的表达。

结果：在 32 个基因中，苦杏仁苷分别在 24 和 48 小时下调了 16 个基因和 19 个基因的表达 > 1.5 倍。在 24 小时时，DNA 聚合酶 α-primase 复合物的下调基因为 POLA1、POLA2、PRIM1 和 PRIM2；DNA聚合酶δ复合物：POLD3；DNA 聚合酶 ε 复合物：POLE4、微染色体维持蛋白 (MCM) 复合物（解旋酶）：MCM2、MCM3、MCM4、MCM6 和 MCM7；夹具和夹具装载器：PCNA；核酸酶：FEN1；和 DNA 连接酶：LIG1。在 48 小时时，DNA 聚合酶 α-引物酶复合物的下调基因为 POLA1、POLA2 和 PRIM1；DNA聚合酶δ复合物：POLD3；DNA聚合酶ε复合物：POLE和POLE2；MCM复合体（解旋酶）：MCM2、MCM3、MCM4、MCM5、MCM6和MCM7；夹具和夹具加载器：PCNA、RFC2 和 RFC3；RNase H：RNASEH2A；核酸酶：DNA2 和 FEN1；和 DNA 连接酶：LIG1。

结论：苦杏仁苷处理导致在 MCF-7 细胞系中在 DNA 复制中起关键作用的几个基因的下调。因此，它可能用作抗癌剂。