Garlic and associated allyl sulfur components inhibit N-methyl-N-nitrosourea induced rat mammary carcinogenesis

Schaffer, Eric; Liu, Jinzhou; Green, Jeffrey; Dangler, Charles A.; Milner, John A.

doi:10.1016/0304-3835(96)04160-2

Cited by 129 publications

(60 citation statements)

References 21 publications

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“…12) Garlic and associated allyl sulfur compounds, water-soluble S-allyl cysteine and oil-soluble diallyl disulfide, are effective inhibitors of mammary carcinogenesis induced by N-methyl-Nnitrosourea in rats. 13) Garlic oil topically applied in the initiating phase of benzo(a)pyrene-induced skin carcinogenesis decreases the number of mice with skin tumors, together with the mean number of tumors per mouse. 14) Allyl methyl disulfide may induce an increase of glutathione S-transferase activity and inhibit tumor development in both forestomach and lungs.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Allium Vegetables against Both Esophageal and Stomach Cancer: A Simultaneous Case‐referent Study of a High‐epidemic Area in Jiangsu Province, China

Gao

Takezaki

Ding

et al. 1999

Japanese Journal of Cancer Research

166

103

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Allium Vegetables against Both Esophageal and Stomach Cancer: A Simultaneous Case‐referent Study of a High‐epidemic Area in Jiangsu Province, China

Gao

Takezaki

Ding

et al. 1999

Japanese Journal of Cancer Research

166

103

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“…Intragastric intubation of DADS provided protection against colon and renal neoplasia in a multiorgan carcinogenesis model in male F344 rats (Takahashi et al, 1992). Cancer chemoprevention by naturally occurring OSC analogues has also been observed against N-nitrosomethylbenzylamine-induced esophageal cancer in rats (Wargovich et al, 1988), dimethylhydrazine-induced colon cancer in mice (Wargovich, 1987;Sumiyoshi and Wargovich, 1990), benzo [a]pyrene-induced forestomach and pulmonary carcinogenesis in mice (Sparnins et al, 1988), and Nmethyl-N-nitrosourea and 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine-induced mammary cancer in rats (Schaffer et al, 1996;Suzui et al, 1997).…”

Section: Introductionmentioning

confidence: 97%

“…Garlic-derived OSCs, including diallyl sulfide (DAS), diallyl disulfide (DADS) and diallyl trisulfide (DATS), have been shown to offer significant protection against cancer in animal models induced by a variety of chemical carcinogens (Wargovich, 1987;Sparnins et al, 1988;Wargovich et al, 1988;Wattenberg et al, 1989;Sumiyoshi and Wargovich, 1990;Takahashi et al, 1992;Reddy et al, 1993;Schaffer et al, 1996;Suzui et al, 1997). For example, N-nitrosodiethylamine-induced neoplasia of the forestomach in mice was inhibited significantly by DADS administration (Wattenberg et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Diallyl trisulfide-induced apoptosis in human prostate cancer cells involves c-Jun N-terminal kinase and extracellular-signal regulated kinase-mediated phosphorylation of Bcl-2

et al. 2004

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Garlic-derived organosulfides (OSCs) including diallyl trisulfide (DATS) are highly effective in affording protection against chemically induced cancer in animals. Evidence is also mounting to indicate that some naturally occurring OSCs can suppress proliferation of cancer cells by causing apoptosis, but the sequence of events leading to proapoptotic effect of OSCs is poorly defined. Using PC-3 and DU145 human prostate cancer cells as a model, we now demonstrate that DATS is a significantly more potent apoptosis inducer than diallyl sulfide (DAS) or diallyl disulfide (DADS). DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2, reduced Bcl-2 : Bax interaction, and cleavage of procaspase-9 and -3. Bcl-2 overexpressing PC-3 cells were significantly more resistant to apoptosis induction by DATS compared with vector-transfected control cells. DATS treatment resulted in activation of extracellular-signal regulated kinase 1/2 (ERK1/2) and cjun N-terminal kinase 1 (JNK1) and/or JNK2, but not p38 mitogen-activated protein kinase. Phosphorylation of Bcl-2 in DATS-treated PC-3 cells was fully blocked in the presence of JNK-specific inhibitor SP600125. Moreover, JNK inhibitor afforded significant protection against DATS-induced apoptosis in both cells. DATS-induced Bcl-2 phosphorylation and apoptosis were partially attenuated by pharmacological inhibition of ERK1/2 using PD98059 or U0126. Overexpression of catalase inhibited DATS-mediated activation of JNK1/2, but not ERK1/2, and apoptosis induction in DU145 cells suggesting involvement of hydrogen peroxide as a second messenger in DATSinduced apoptosis. In conclusion, our data point towards important roles for Bcl-2, JNK and ERK in DATS-induced apoptosis in human prostate cancer cells.

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“…Garlic-derived OSCs including diallyl sulfide (DAS), diallyl disulfide (DADS) and diallyl trisulfide (DATS) have been shown to offer significant protection against cancer in animal models induced by a variety of chemical carcinogens (Wargovich, 1987;Sparnins et al, 1988;Wargovich et al, 1988;Wattenberg et al, 1989;Sumiyoshi and Wargovich, 1990;Takahashi et al, 1992;Reddy et al, 1993;Schaffer et al, 1996;Suzui et al, 1997). For example, cancer chemoprevention by naturally occurring OSC analogues has been observed against benzo [a]pyrene-induced forestomach and pulmonary carcinogenesis in mice (Sparnins et al, 1988), N-nitrosomethylbenzylamine-induced esophageal cancer in rats (Wargovich et al, 1988), and 1,2-dimethylhydrazine-induced colon cancer in mice (Sumiyoshi and Wargovich, 1990).…”

Section: Introductionmentioning

confidence: 99%

Diallyl trisulfide-induced G2–M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc25C

Xiao

Herman-Antosiewicz²,

Antosiewicz³

et al. 2005

Oncogene

177

195

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Molecular mechanism of cell cycle arrest caused by diallyl trisulfide (DATS), a garlic-derived cancer chemopreventive agent, has been investigated using PC-3 and DU145 human prostate cancer cells as a model. Treatment of PC-3 and DU145 cells, but not a normal prostate epithelial cell line (PrEC), with growth suppressive concentrations of DATS caused enrichment of the G 2 -M fraction. The DATS-induced cell cycle arrest in PC-3 cells was associated with increased Tyr 15 phosphorylation of cyclin-dependent kinase 1 (Cdk1) and inhibition of Cdk1/cyclinB1 kinase activity. The DATStreated PC-3 and DU145 cells also exhibited a decrease in the protein level of Cdc25C and an increase in its Ser 216 phosphorylation. The DATS-mediated decrease in protein level and Ser 216 phosphorylation of Cdc25C as well as G 2 -M phase cell cycle arrest were significantly attenuated in the presence of N-acetylcysteine implicating reactive oxygen species (ROS) in cell cycle arrest caused by DATS. ROS generation was observed in DATS-treated PC-3 and DU145 cells. DATS treatment also caused an increase in the protein level of Cdk inhibitor p21, but DATS-induced G 2 -M phase arrest was not affected by antisense-mediated suppression of p21 protein level. In conclusion, the results of the present study indicate that DATS-induced G 2 -M phase cell cycle arrest in human prostate cancer cells is caused by ROS-mediated destruction and hyperphosphorylation of Cdc25C.

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Garlic and associated allyl sulfur components inhibit N-methyl-N-nitrosourea induced rat mammary carcinogenesis

Cited by 129 publications

References 21 publications

Protective Effect of Allium Vegetables against Both Esophageal and Stomach Cancer: A Simultaneous Case‐referent Study of a High‐epidemic Area in Jiangsu Province, China

Protective Effect of Allium Vegetables against Both Esophageal and Stomach Cancer: A Simultaneous Case‐referent Study of a High‐epidemic Area in Jiangsu Province, China

Diallyl trisulfide-induced apoptosis in human prostate cancer cells involves c-Jun N-terminal kinase and extracellular-signal regulated kinase-mediated phosphorylation of Bcl-2

Diallyl trisulfide-induced G2–M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc25C

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