Diallyl disulfide-induced G2/M arrest of human gastric cancer MGC803 cells involves activation of p38 MAP kinase pathways

Yuan, Juan; Wang, Guihua; Ling, Hui; Qi, Shijie; Yang, Yuehong; Song, Ying; Tang, Rongjun; Liu, Yao; Huang, Chen

doi:10.3748/wjg.v10.i18.2731

Cited by 56 publications

(47 citation statements)

References 34 publications

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“…recent studies have reported that the ability of dadS to up-or down-regulate the mrna expression of some genes is related to its signal pathway (17)(18)(19)(20)46). our results revealed that dadS may be involved in mediating multiple signal pathways in HT-29 cells by up-regulating the expression of GPCR175, GNB1, PSMD12, S100A6, TACSTD2 or by suppressing ATP1A1, YWHAE and FLJ25150 fis.…”

Section: Discussionsupporting

confidence: 51%

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Huang

Xie

et al. 2011

Mol Med Rep

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Abstract. diallyl disulfide (dadS), a sulfur compound derived from garlic, has been shown to have protective effects against colon carcinogenesis in several studies performed in rodent models. However, its molecular mechanism of action remains unclear. This study was designed to confirm the antiproliferative activity of dadS and to screen for differentially expressed genes induced by dadS in human colon cancer cells with the aim of exploring its possible anticancer mechanisms. The anti-proliferative capability of dadS in the HT-29 human colon cancer cells was analyzed by MTT assays and flow cytometry. The differences in gene expression between dadStreated (experimental group) and untreated (control group) HT-29 cells were identified using two-directional suppression subtractive hybridization (SSH). Semi-quantitative reverse transcription polymerase chain reaction (semi-rT-Pcr) was selected to confirm the results obtained by SSH. Based on the results, a dose-and time-dependent growth inhibition was observed in the dadS-treated HT-29 cells. Forty-nine known genes and a new gene were found to be involved in the anti-proliferative effects of dadS by SSH analysis, and two cdna libraries, dHdG and dHuG, containing both up-and down-regulated genes in colon tumor cells, were constructed. These genes were related to transduction, cell proliferation/ growth/apoptosis and secreted/extracellular matrix proteins. Semi-rT-Pcr results showed an expression pattern consistent with that of the SSH analysis. in conclusion, dadS showed anti-proliferative effects on colon cancer HT-29 cells, and dHdG and dHuG genes were found to be involved in this process. Further studies on the identification and description of these genes may allow a better understanding of the protective roles of dadS in colon carcinogenesis. Introductioncolon cancer is one of the major causes of cancer death worldwide (1). an understanding of the mechanisms involved in the occurrence and development of colon cancer would aid in its therapy. epidemiological investigations have provided compelling evidence that environmental factors are modifiers in colon cancer (1-3); diet has also been shown to be an important determinant of cancer risk and tumor behavior (3-5).Garlic consumption is very popular all over the world. epidemiological studies have shown an inverse correlation between the consumption of garlic and colon cancer in certain areas (6). Many in vivo experiments have revealed the antitumorigenic activity of garlic or of allyl sulfur compounds from garlic (7-17).Diallyl disulfide (DADS) is the major component of cooked garlic and an oil-soluble organosulfur compound in processed garlic that inhibits the proliferation of several human cancer cells, including breast (11), hepatoma (12), colon cancer (13) and human leukemia . Previous studies from our laboratory revealed that dadS suppresses gastric (15) and colon cancer (16). additionally, leukemia cell proliferation was related to dadS (14,17), possibly because of its ability to induce cell cycle arrest and...

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Section: Discussionsupporting

confidence: 51%

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Huang

Xie

et al. 2011

Mol Med Rep

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“…A decreased Cdc25C expression plays a crucial role in G 2 /M arrest after treatment with DADS (19). In the current study, DADS was shown to induce phosphorylation of ATR (ATM-RAD3-related gene) and Chk, while suppressing expression of Cdc25C and cyclin B1 in the human gastric cancer cell line BGC823.…”

Section: Introductionmentioning

confidence: 74%

“…The MTT assay was performed using the method of Yuan et al (19). Briefly, a 200-μL suspension containing approximately 2 x 10 4 cells was added to each well of a 96-well culture plate and incubated for 24 h at 37°C in a humidified atmosphere of 95% air and 5% CO 2 .…”

Section: Cell Viability Assaymentioning

confidence: 99%

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Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide

Ling

Wen

et al. 2010

Braz J Med Biol Res

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“…Recent studies indicate that diallyldisulfide and, in some cases diallyltrisulfide, cause mitotic arrest in cancer cells (7)(8)(9). Interestingly, these organosulphur compounds do not only inhibit cancer cell proliferation but also appear to induce apoptosis in cancer cells, which apart from chemo-preventive aspects turns these agents into interesting lead structures for the treatment of already existing cancers (10-13).…”

Section: Introductionmentioning

confidence: 99%

Diallylpolysulfides induce growth arrest and apoptosis

Busch

Jacob²,

Ali³

et al. 2010

Int J Oncol

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Abstract. Garlic-derived organo sulphur compounds such as diallylsulfides provide a significant protection against carcinogenesis. Chemically synthesized, and highly pure diallylsulfides with a chain of 1-4 sulphur atoms, as well as a range of control compounds, were employed to investigate the influence of these agents on cell viability, cell cycle arrest and induction of apoptosis in HCT116 human colon cancer cells. Diallyltrisulfide, and even more efficiently diallyltetrasulfide treatment of HCT116 cells led to a reduced cell viability, cell cycle arrest and apoptosis. A similar activity was found for the propylanalogues, while mono-and disulfides were considerably less active. Initial calculations point toward the ability of triand tetrasulfides to form reactive oxygen species (ROS). Here, we found that the induction of apoptosis was indeed dependent on the redox-state of the cell, with anti-oxidants being able to prevent sulfide-induced apoptosis. Furthermore, using HCT116 cells which were either positive or negative for p53 revealed that p53 is clearly dispensable for induction of apoptosis. Growth arrest and induction of apoptosis is associated with a considerable reduction of the level of cdc25C. These results support the therapeutic potential of polysulfides and allow insight into the mechanisms based on the polysulfide biochemistry.

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Diallyl disulfide-induced G2/M arrest of human gastric cancer MGC803 cells involves activation of p38 MAP kinase pathways

Abstract: DADS-induced G2/M arrest of MGC803 cells involves activation of p38 MAP kinase pathways. Decreased Cdc25C protein expression by p38 MAPK played a crucial role in G2/M arrest after treatment with DADS.

Cited by 56 publications

References 34 publications

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide

Diallylpolysulfides induce growth arrest and apoptosis

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