• 한국식품영양학회지
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• 제30권2호
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• pp.191-202
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• 2017

This study was conducted to investigate the characteristics of major prebiotics and the related studies, and to provide basic data for future research. Prebiotics are defined as 'nondigestible food ingredients that beneficially affect the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, and thus improve host health'. Well-known prebiotics are inulin, oligofructose, and galacto-oligosaccharide. Prebiotics assist in the health activity of lactic acid bacteria by acting as a substrate for lactic acid bacteria, with their unique physical and chemical properties. Bifidobacteria are known to be beneficial bacteria that prevent intestinal inflammation, maintain intestinal microflora balance, inhibit carcinogenesis, reduce cholesterol, and enhance immunity. However, Bifidobacteria, Lactobacillus, Bacillus, and Weissella are also found in animal-based fermented foods such as milk, cheese, yogurt, and salted fish. Prebiotics can act as a substrate for lactic acid bacteria, helping the activity of lactic acid bacteria and improving health. Therefore, the authors suggest that investigation into the category and effectiveness of prebiotics should be extended in the future through research.

• Asian Pacific Journal of Cancer Prevention
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• 제13권6호
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• pp.2429-2435
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• 2012

Methyl isocyanate may have a role in cancer etiology, although the link is unclear. There is evidence in the literature that it can induce cancer in animals but the carcinogenic potency is weak. Pheochromocytoma of adrenal medulla and acinar cell tumors of pancreas have been observed in methyl isocyanate exposed animals. Conversely, emerging data from population-based epidemiological studies are contradictory since there is no evidence of such cancers in methyl isocyanate exposed humans. Recently, we reported a high prevalence of breast and lung cancers in such a population in Bhopal. In vitro findings appearing in the latest scientific literature suggest that genomic instability is caused by methyl isocyanate analogs in lung, colon, kidney, ovary epithelial cells, and that hepatocytes may undergo oncogenic transformation, have obvious implications. The conflicting information prompted us to present this update over the last three decades on methyl isocyanate-induced cancers after an extensive literature search using PubMed. While the pertinent literature remains limited, with a scarcity of strong laboratory analyses and field-epidemiological investigations, our succinct review of animal and human epidemiological data including in vitro evidences, should hopefully provide more insight to researchers, toxicologists, and public health professionals concerned with validation of the carcinogenicity of methyl isocyanate in humans.

• Asian Pacific Journal of Cancer Prevention
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• 제15권16호
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• pp.6787-6790
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• 2014

Background: The aim of this study was to evaluate cyclooxygenase-2 (COX-2) immunoreactivity in colorectal adenocarcinomas and to find correlations with different pathological features. Materials and Methods: This study included 35 cases of colorectal carcinoma foir which surgical colectomy specimens were collected. Immunohistochemical staining of COX-2 (cyclooxygenase-2) is done by using the Streptavidin-biotin technique. Results: This work reveals that COX-2 is positive in most cases of colorectal carcinoma and negative in normal colon tissue with statistically non significant relations between COX-2 immunostaining and different pathological features. Conclusions: Our data suggest over expression of COX-2 protein in colorectal carcinoma in contrast to normal mucosa, with a possible role in cell proliferation in carcinogenesis.

• 한국수의병리학회:학술대회논문집
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• 한국수의병리학회 2000년도 추계학술대회 및 정기총회
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• pp.26-26
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• 2000

The consumption of cruciferous vegetables such as cabbage and broccoli have been shown to have a chemopreventive effect in human and in experimental animals. Indole-3-carbinol (I3C), one component of cruciferous vegetables, has been shown to exert its chemopreventive effect in liver, colon and mammary tissue before or concurrent exposure of carcinogen, but in some reports, there have been several evidence that consumption of I3C after carcinogen treatment induced tumor promotion in some tissues. There have been no reports about the effect of I3C after carcinogen exposure in N-Nitroso-N-methylurea (MNU)-induced mammary tumor model of rats. (omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.85-86
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• 2001

Indole-3-carbinol (I3C), one component of cruciferous vegetables (the Family of Cruciferae), has been shown to exert chemopreventive effects in liver, colon and mammary tissue, but there has been substantial evidence that consumption of I3C induces tumor promotion in some tissues. Our studies were investigated to examine the modifying effects of I3C in the 7, 12-dimethylbenz［a］anthracene (DMBA) induced rat mammary tumor model.(omitted)

• BMB Reports
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• 제51권3호
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• pp.119-125
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• 2018

The Hippo pathway plays prominent and widespread roles in various forms of human carcinogenesis. Specifically, the Yes-associated protein (YAP), a downstream effector of the Hippo pathway, can lead to excessive cell proliferation and the inhibition of apoptosis, resulting in tumorigenesis. It was reported that the YAP is strongly elevated in multiple types of human malignancies such as breast, lung, small intestine, colon, and liver cancers. Recent work indicates that, surprisingly, Hippo signaling components' (SAV1, MST1/2, Lats1/2) mutations are virtually absent in human cancer, rendering this signaling an unlikely candidate to explain the vigorous activation of the YAP in most, if not all human tumors and an activated YAP promotes the resistance to RAF-, MAPK/ERK Kinase (MEK)-, and Epidermal growth factor receptor (EGFR)-targeted inhibitor therapy. The analysis of YAP expressions can facilitate the identification of patients who respond better to an anti-cancer drug treatment comprising RAF-, MEK-, and EGFR-targeted inhibitors. The prominence of YAP for those aspects of cancer biology denotes that these factors are ideal targets for the development of anti-cancer medications. Therefore, our report strongly indicates that the YAP is of potential prognostic utility and druggability in various human cancers.

• 대한수의학회지
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• 제41권4호
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• pp.549-555
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• 2001

Indole-3-carbinol (I3C), one component of cruciferous vegetables (the Fammily of Cruciferae), has been shown to exert its chemopreventive effect in liver, colon and mammary tissue before or concurrent exposure of carcinogen, but there have been several evidences that consumption of I3C induced tumor promotion in some tissues. Our studies were investigated to examine the modifying effects of I3C in the 7,12-dimethylbenz[$\alpha$]anthracene (DMBA) induced rat mammary gland tumor model. Fifty-two female Sprague-Dawley rats were randomly divided into five groups. Animals of the group 1 were given the diet containing 100ppm I3C and animals of the groups 2 and 4 were given the diet containing 300ppm I3C from 6 weeks of age. At 7 weeks of age, the animals of the groups 1, 2 and 3 were intubated with DMBA. All amimals were killed at 20 weeks after carcinogen treatment. There were significant increases of food consumption in I3C feeding groups compared with those of basal diet feeding groups. The incidences of the mammary tumors in the group 1, 2 and 3 were 75.0% (9/12), 56.3% (9/16) and 93.8% (15/16), respectively and the average number of tumors of group 1 (DMBA+I3C 100ppm: $2.08{\pm}0.61$) and 2 (DMBA+I3C 300ppm: $1.19{\pm}0.32$) were significantly lower than that of group 3 (DMBA alone: $4.63{\pm}0.72$) at the value of P<0.05 and P<0.001, respectively. In the pathological examination of appearing tumors, most of them were adenocarcinoma. Many epithelial cells of tumors showed strong estrogen receptor (ER) $\alpha$ expression but there were slight difference of ER $\alpha$ expression among the type of tumors. We suggest that pre-initiation treatment of I3C has an inhibitory effects on mammary carcinogenesis induced by DMBA.

• Journal of Nutrition and Health
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• 제29권1호
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• pp.112-121
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• 1996

The study was designed to observe the effect of blend fat calculated from the foods consumed in Korean with those of perilla oil, beef tallow and corn oil on colonic mucosal phospholipid fatty acid composition and the levels of TXB2 and diacylglycerol (DAG) which were known as biomarkers for cancer. Male Sprague Dawley rats, at 7 weeks of age, were divided into control and 1, 2-dimethylhydrazine (DMH)-treated group, and each group was subdivided into four groups. The experimental diets contained one of four dietary fats, blend fat (BF), perilla oil(PO), beef tallow (BT) or corn oil (CO), at 15% (w/w) level. At the same time, each rat was injected with saline for control group or DMH twice a week for 6 weeks to give total dose of 180mg/kg body weight. DMH injection, regardless of the type of dietary fats, significantly increased the levels of PGE2 and TXB2 in colonic mucosal layer compared to control (p<0.01). However, the level of eicosanoids was influenced by the types of dietary fats in both control and DMH group. In control groups, colonic mucosal level of TXB2 was higher in beef tallow group, but lower in perilla oil group compared to that of blend fat (p<0.01). In DMH groups, the level of TXB2 was higher in beef tallow and corn oil groups(p<0.05). The level of PGE2 showed the same trends with TXB2 and beef tallow most significantly increased the level of PGE2. DMH treatment did not influence on tissue fatty acid profile, which was directly reflected by dietary fatty acid composition. Proportions of C18 : 2 in colonic mucosal phospholipid well reflected dietary level of C18 : 2 showing the order CO>BF>PO>BT. The precentage of arachidonic acid(AA) in mucosal phospholipid was the highest by CO adn BT groups and the lowest by PO group. The incorporation of $\alpha$-linolenic acid in colonic mucosal phospholipid in perilla oil group was negatively correlated to the content of AA. Dietary level of C18 : 2 might not be the only controlling factor for the production of eicosanoids in colonic mucosa layer and might function with $\omega$3 fatty acids. The level of DAG was significanlty lower in PO group than that of BT group. Therefore, $\omega$3 $\alpha$-linolenic acid rich perilla oil could be very important dietary sourec in controlling eicosanoid production DAG level in cloln and recommenced to use more often in meal preparation to reduce the risk factor against colon cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제17권2호
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• pp.743-748
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• 2016

Background: $K^-Ras$ activation is an early event in colorectal carcinogenesis and associated mutations have been reported in about 40% of colorectal cancer patients. These mutations have always been responsible for enhancing malignancy and silencing them is associated with attenuation of tumorigenicity. Among downstream effectors are the RAF/MEK/ERK and the PI3K/Akt signaling pathways. PI3K/Akt signaling leads to reduction of apoptosis, stimulated cell growth and enhanced proliferation. Ellagic acid (EA), a naturally occurring antioxidant, has recently emerged as a promising anti-cancer agent. Purpose: To evaluate the impact of cellular genetic makeup of two colon cancer cell lines with different genetic backgrounds, HCT-116 ($K^-Ras^-/p53^+$) and Caco-2 ($K^-Ras^+/p53^-$), on response to potential anti-tumour effects of EA. In addition, the influence of $K^-Ras$ silencing in HCT-116 cells was investigated. Materials and Methods: Cellular proliferation, morphology and cell cycle analysis were carried out in addition to Western blotting for detecting total Akt and p-Akt (at Thr308 and Ser473) in the presence and absence of different concentrations of EA. Cell proliferation was also assessed in cells transfected with different concentrations of $K^-Ras$ siRNA or incubated with ellagic acid following transfection. Results: The results of the present study revealed that EA exerts anti-proliferative and dose-dependent pro-apoptotic effects. Cytostatic and cytotoxic effects were also observed. p-Akt (at Thr308 and Ser473) was downregulated. Moreover, EA treatment was found to (i) reduce $K^-Ras$ protein expression; (ii) in cells transfected with siRNA and co-treated with EA, pronounced anti-proliferative effects as well as depletion of p-Akt (at Thr308) were detected. Conclusions: Cellular genetic makeup ($K^-Ras^-/p53^-$) was not likely to impose limitations on targeting EA in treatment of colon cancer. EA had a multi-disciplinary pro-apoptotic anti-proliferative approach, having inhibited Akt phosphorylation, induced cell cycle arrest and showed an anti-proliferative potential in HCT-116 cells (expressing mutant $K^-Ras$).

• Molecules and Cells
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• 제37권12호
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• pp.899-906
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• 2014

Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.