• Journal of Life Science
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• v.20 no.4
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• pp.561-571
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• 2010

Colon cancer is one of the most common malignancies in the western world and the second leading cause of cancer death in Korea. Epidemiology studies have shown a reduced incidence of colon cancer among populations consuming a large quantity of ${\omega}3$-polyunsaturated fatty acids (${\omega}3$-PUFA) of marine origin. Recently, it has been found that ${\omega}3$-PUFA has an antineoplastic effect in several cancers. This study was designed to investigate the mechanism of the anti-invasive effect of ${\omega}3$-PUFA in colon cancer. ${\omega}3$-PUFA, docosahexaenoic acids (DHA) and eicosapentaenoic acid (EPA) treatment resulted in a dose-dependent inhibition of cell growth in SW480 human colon cancer cells. In contrast, arachidonic acid (AA), a ${\omega}6$-PUFA, exhibited no significant effect. This action likely involves apoptosis, given that DHA treatment increased apoptotic cells in TUNEL assay. Moreover, invasiveness of SW480 cells was inhibited following treatment of DHA in a dose-dependent manner; in contrast, AA had no effect. The levels of MMP-9 and MMP-2 mRNA decreased after DHA pretreatment. MMP-9 and MMP-2 promoter activities were also inhibited by DHA treatment. The levels of NF-kB and p-IkB protein were down-regulated by DHA pretreatment in a dose dependent manner. In addition, DHA inhibited NF-kB promoter reporter activities. These findings suggest that ${\omega}3$-PUFA may inhibit cancer cell invasion by inhibition of MMPs via reduction of NF-kB in colon cancer. In conclusion, ${\omega}3$-PUFA could be used for chemoprevention and treatment of human colon cancer.

• Korean Journal of Food Science and Technology
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• v.44 no.3
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• pp.317-323
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• 2012

This study was performed to elucidate the anticancer activities and the mechanism of chloroform fractions from cultivated Orostachys japonicus (CFCOJ) in human colon cancer cells. CFCOJ markedly decreased viable cell numbers in both a dose-dependent and time-dependent manner within SW480 cells. Cell death induced by CFCOJ increased cell populations in the sub-G1 phase, as well as the formation of apoptotic bodies, nuclear condensation, and induced DNA fragmentation. CFCOJ-induced apoptosis was associated with the activation of initiator caspase-8 and -9, as well as the effector caspase-3. CFCOJ also stimulated Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9. CFCOJ increased the expression of the proapoptotic protein, Bax, and decreased the expression of the antiapoptotic protein, Bcl-2. These results indicate that CFCOJ exert anticancer effects on human colon cancer SW480 cells through a caspase-dependent apoptotic pathway.

• Journal of Marine Bioscience and Biotechnology
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• v.1 no.4
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• pp.305-310
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• 2006

Abnormal activation of the Wnt/${\beta}$-catenin pathway and subsequent up-regulation of ${\beta}$-catenin response transcription (CRT) are associated with the development of colon cancer. Thus, the Wnt/${\beta}$-catenin pathway is an attractive target for chemoprevention and treatment of this cancer. In this study, we used a cell-based screen to identify a methanol extract of Dictyota dichotoma (EDD) that suppresses the Wnt/${\beta}$-catenin pathway without altering the level of ${\beta}$-catenin protein and reduces the expression of cyclin D1, which is a known ${\beta}$-catenin/T cell factor (TCF)-dependent gene. EDD inhibited the growth of various colon cancer cells. Our findings suggest that EDD can potentially be used as a chemopreventive agent against colon cancer.

• Applied Chemistry for Engineering
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• v.24 no.5
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• pp.525-529
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• 2013

Contents of the total polyphenols and flavonoids in the dietary fiber from tubers and stalks of domestic sweet potatoes were investigated. In addition, their antioxidant activity as well as the potent anti-cancer effects through the growth inhibition in human colon cancer cells (HT-29) in vitro were tested. The total flavonoids as naringin equivalents in dietary fiber from tubers and stalks of sweet potatoes were $0.5{\pm}0.001$ naringin/g extract and $2.0{\pm}0.008$ mg naringin/g extract dry basis, respectively. The amounts of the total polyphenols as gallic acid equivalents were $2.8{\pm}0.01$ mg gallic acid/g dry basis and $6.3{\pm}0.03$ mg gallic acid/g dry basis, respectively. 1,2-Diphenyi-1-picrylhydrazyl (DPPH) radical-scavenging activity of the dietary fiber from stalks was 2.4 times higher than that of the dietary fiber from tubers. Interestingly, a strong growth inhibition on HT-29 cells was observed in both dietary fibers originated from stalks and tubers of sweet potato in a dose-dependent manner. In addition, we found that the dietary fiber from tubers and stalks of sweet potato increased the gene expression of tumor suppressor p53. The great potential value in the prevention of various diseases including cancer the potential value could be confirmed through effects of the dietary fiber from tubers and stalks of sweet potato on antioxidant activity and anticancer in human colon cancer.

• Preventive Nutrition and Food Science
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• v.2 no.4
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• pp.348-353
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• 1997

The antimutagenic and cancer cell growth inhibitory effects of methanol extracts from 9 kinds of seaweed were studied in the Ames assay and cell culture systems, respectively. The methanol extracts from the seaweeds of sea lettuce, chlorella, sea tangle, sea mustard, sporophyll of sea mustard, fusiforme, seaweed papulosa, purple laver and ceylon moss showed antimutagenicities against aflatoxin B₁(AFB₁) and N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) in the Salmonella typhimurium TA100. These extracts revealed relatively higher antimutagenicity against AFB₁(indirect mutagen) than MNNG(direct mutagen). Sporophyll of sea mustard and seaweed papulosa exhibited strong antimutagenic activity against AFB₁, and sporophyll of sea mustard, sea tangle and ceylon moss also reduced the mutagenicity induced by MNNG. The sporophyll fo sea mustard exerted the highest antimutagenic activity among the samples treated. The methanol extracts from 9 kinds of seaweed inhibited the growth of two cancer cell lines, AGS human gastric adenocarcinoma cells and HT-29 human colon carcinoma cells. Sea tangle, sea mustard and sporophyll of sea mustard inhibited the growth of cancer cells significantly. These results suggest that various seaweeds show not only antimutagenic activity but also growth inhibitory effect of some cancer cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.2
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• pp.372-376
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• 2001

The effect of garlic extract and vitamin C mixture on the various cancer cell lines in vitro and in vivo have been examined. Proliferation of human colon cancer (HT-29), human rectal cancer (HRT-18) and human hepatoma (HepG2) cells was inhibited by garlic extract and vitamin C, respectively. Based on the cytotoxic activity, mixture of garlic extract and vitamin C was demonstrated to possess a synergistic growth inhibition on HT-29, HRT-18 and HepG2 cancer cells. Mixture of garlic extract and vitamin C significantly arrested G2/M phase cells in the HepG2 cell cycle. Oral administration of mixture of garlic extract and vitamin C to sarcoma-180 tumor-bearing mice prolonged survival time compared to that of control group. These results suggested that addition of vitamin C enhances anticancer activity of garlic extract in vitro, and mixture of garlic extract and vitamin C has antitumor effect in vivo.

• Journal of Life Science
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• v.27 no.9
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• pp.1020-1030
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• 2017

Epidemiology studies have reported a reduced incidence of colon cancer among populations that consume a large quantity of ${\omega}3-polyunsaturated$ fatty acids (${\omega}3-PUFAs$) of marine origin. Herein, we demonstrated a mechanism of anticancer action of ${\omega}3-PUFAs$, showing that they suppressed invasion and tumorigenicity in colon cancer cells. Docosahexaenoic acids (DHA) inhibited the cell growth of HT29 cells. This action likely involved apoptosis, given that the DHA treatment increased the cleaved form of PARP and sub G1 cells. Moreover, the invasiveness of HT29 cells was inhibited following DHA treatment, whereas arachidonic acid (AA) had no effect. The levels of Matrix-metalloproteinase-9 (MMP-9) and MMP-2 mRNA decreased after DHA pretreatment. DHA treatment inhibited MMP-9 and MMP-2 promoter activities and reduced VEGF promoter activity. DHA pretreatment also inhibited the activities of prostaglandin-2 (PGE2)-induced MMPs and the VEGF promoter. Cyclooxygenase-2 (COX-2) overexpression increased the activity of MMPs and that of the Vascular endotherial growth factor (VEGF) promoter in HT29 cells, and DHA inhibited NF-kB and COX-2 promoter reporter activities. As shown by in vivo experiments, when mouse colon cancer cells (MCA38) were implanted into Fat-1 and wild-type mice, both the tumoral size and volume were dramatically inhibited in Fat-1 transgenic mice. Furthermore, TUNEL-positive cells increased in tumors from Fat-1 mice compared with wild mice. In immunohistochemistry, the intensity of CD31 in Fat-1 tumors was weaker. These findings suggest that ${\omega}3-PUFAs$ may inhibit tumorigenicity and angiogenesis as well as cancer cell invasion by suppression of COX-2, MMPs and VEGF via the reduction of NF-kB in colon cancer.

• Journal of Ginseng Research
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• v.20 no.3
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• pp.219-225
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• 1996

This study was performed to investigate the inhibition mechanism of cancer cell proof iferation caused by the petroleum-ether extract of ginseng against human rectum (HRT-18), colon (HT-29), llepatoma (Hep G2) and prostate (LNCaP) cancer cells and monkey kidney cells (Vero 76). Cells were treated with the petroleum-ether extract of ginseng (50 to 200 $\mu\textrm{g}$/ml) in G1 or S phase of the cell cycle, and proliferation and protein kinase C activity were measured. The petroleum-eth or extract of ginseng inhibited proliferation of HRT-18, HT-29, Hep G2 and LNCaP when treated in Gl phase, but not in S phase. This result shows that the ginseng extract arrests the cell cycle in G1 phase, resulting in the inhibition of cell proliferation. At the same concentrations, treatment of the ginseng extract in G1 phase decreased protein kinase C activity, while the treatment in S phase had no effect. This reault suggests that protein kinase C might be involved in the inhibition of the cell cycle and proliferation of cancer cells caused by the petroleum-ether extract of ginseng.

• Archives of Pharmacal Research
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• v.22 no.2
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• pp.151-156
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• 1999

Despite the impressive antitumor activity of cisplatin, two major limitations of the drug, that is severe side effects and drug-resistance of cancer cells, make its use difficult of r cancer therapy. These limitations have resulted in a greate deal of effort having been expended into structural modifications of cisplatin. In this study, we tested two novel cisplatin analogues, (CPA)2 Pt[DOLYM] (COMP-I) and (DACH)Pt[DOLYM] (CoMP-II), for the mode of cytotoxic action against human tumor cells comparing with cisplatin and carboplatin in vitro. These two novel analogues had considerable cytotoxic activities against five kinds of human solid tumor cells, and especially COMP-II was more effective on HCT15 colon cancer cells than other compounds. In addition, COMP-II had cytostatic activity at low concentrations (10~0.3${\mu}g/ml$), but other compounds revealed little effect on tumor growth at the low concentration.

• Journal of Nutrition and Health
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• v.41 no.1
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• pp.13-21
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• 2008

To determine whether indol-3-carbinol (BC, $C_9H_9NO$), an autolysis product of a glucosinolate and a glucobrassicin in vegetables, regulated tight junction proteins (TJ) and suppressed cell invasion in colon cancer cells, this experiment was performed. Our results indicate that I3C inhibit cell growth of HT-29 cells in a dose (0, 50, $100{\mu}M$) and time (0, 24 and 48h) dependent manner. Using the wound healing and matrigel invasion study, respectively, BC inhibits the cell motility and invasion of the ovarian cancer cell line. The TEER values were increased in HT-29 cells grown in transwells treated with BC, reversely, paracellular permeability was decreased in those of condition. Claudin-1, claudin-5, ZO-1 and occuldin have been shown to be positively expressed in HT-29 coloncancer cells. I3C occurs concurrently with a significant decrease in the levels of those of proteins in HT-29 cells. But E-cadherin level in the HT-29 was increased by I3C. The reduction of claudin-1 and claudin-5 protein levels occurred post-transcriptionaly since their mRNA levels are no difference by I3C. Therefore, our results suggest that I3C may be expected to inhibit cancer metastasis and invasion by tighten the cell junction and restoring tight junction in colon cancer cell line, HT-29.