Amygdalin inhibits genes related to cell cycle in SNU-C4 human colon cancer cells

Figure 1 Reverse-phase HPLC separation of amygdalin by phosphate buffer. (A) D-amygdalin standard. (B) D-amygdalin obtained by our method; peaks: 1, neoamygdalin; 2, D-amygdalin.

Figure 2 Cytotoxicity of amygdalin. SNU-C4 human colon cancer cells were treated with various concentrations (0.25, 0.5, 2.5, and 5 mg/mL) of amygdalin for 24 h prior to the determination of cellular viability through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Independent experiment was repeated thrice. Results are presented as mean±SE (bP<0.01 vs control group).

Figure 3 Expression pattern in a 8k human cDNA microarray.

Figure 4 Scattered plot of the normalization results by global M method.

Figure 5 Confirmation of cDNA microarray results of downregulated genes by RT-PCR. Five genes, exonuclease 1 (EXO1), ABC, sub-family F (GCN20), member 2 (ABCF2), MRE11 meiotic recombination 11 homolog A (MRE11A), topoisomerase (DNA) I (TOP1), and FK506 binding protein 12-rapamycin associated protein 1 (FRAP1), were analyzed by RT-PCR with total RNA from control and amygdalin (5 mg/mL, 24 h)-treated human colon cancer cells. As an internal control, CYCLOPHILN was amplified.