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. 2005 Sep 7;11(33):5156-61.
doi: 10.3748/wjg.v11.i33.5156.

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

Hae-Jeong Park  1 , Seo-Hyun Yoon, Long-Shan Han, Long-Tai Zheng, Kyung-Hee Jung, Yoon-Kyung Uhm, Je-Hyun Lee, Ji-Seon Jeong, Woo-Sang Joo, Sung-Vin Yim, Joo-Ho Chung, Seon-Pyo Hong
Affiliations

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

Hae-Jeong Park et al. World J Gastroenterol. .

Abstract

Aim: The genes were divided into seven categories according to biological function; apoptosis-related, immune response-related, signal transduction-related, cell cycle-related, cell growth-related, stress response-related and transcription-related genes.

Methods: We compared the gene expression profiles of SNU-C4 cells between amygdalin-treated (5 mg/mL, 24 h) and non-treated groups using cDNA microarray analysis. We selected genes downregulated in cDNA microarray and investigated mRNA levels of the genes by RT-PCR.

Results: Microarray showed that amygdalin downregulated especially genes belonging to cell cycle category: exonuclease 1 (EXO1), ATP-binding cassette, sub-family F, member 2 (ABCF2), MRE11 meiotic recombination 11 homolog A (MRE11A), topoisomerase (DNA) I (TOP1), and FK506 binding protein 12-rapamycin-associated protein 1 (FRAP1). RT-PCR analysis revealed that mRNA levels of these genes were also decreased by amygdalin treatment in SNU-C4 human colon cancer cells.

Conclusion: These results suggest that amygdalin have an anticancer effect via downregulation of cell cycle-related genes in SNU-C4 human colon cancer cells, and might be used for therapeutic anticancer drug.

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Figures

Figure 1
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
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
Figure 3
Expression pattern in a 8k human cDNA microarray.
Figure 4
Figure 4
Scattered plot of the normalization results by global M method.
Figure 5
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.
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