• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6017-6022
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• 2012

Background: Resveratrol has been reported to have potential chemopreventive and apoptosis-inducing properties in a variety of tumor cell lines. Objective: In this study, to investigate the effects of resveratrol on protein kinase C (PKC) activity and apoptosis in human colon carcinoma cells, we used HT-29 cells and examined the $PKC{\alpha}$ and ERK1/2 signaling pathways. Methods: To test the effects of resveratrol on the growth of HT-29 cells, the cells were exposed to varying concentrations and assessed with the the MTT cell-viability assay. Fluorescence-activated cell sorter (FACS) analysis was applieded to determine the effects of resveratrol on cell apoptosis. Western blotting was performed to determine the protein levels of $PKC{\alpha}$ and ERK1/2. In inhibition experiments, HT-29 cells were treated with G$\ddot{o}$6976 or PD98059 for 30 min, followed by exposure to $200{\mu}M$ resveratrol for 72 h. Results: Resveratrol had a significant inhibitory effect on HT-29 cell growth. FACS revealed that resveratrol induced apoptosis. Western blotting showed that e phosphorylation of $PKC{\alpha}$ and ERK1/2 was significantly increased in response to resveratrol treatment. Pre-treatment with $PKC{\alpha}$ and ERK1/2 inhibitors (G$\ddot{o}$6976 and PD98059) promoted apoptosis. Conclusion: Resveratrol has significant anti-proliferative effects on the colon cancer cell line HT-29. The PKC-ERK1/2 signaling pathway can partially mediate resveratrol-induced apoptosis of HT-29 cells.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.229.1-229.1
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• 2003

The anti proliferative effects of bile acids and their derivatives on HT -29 human colon cancer cells were investigated. Ursodeoxycholic acid (UDCA) and its synthetic derivatives, HS-1030 and HS-1183, and chenodeoxycholic acid (CDCA) and its synthetic derivatives, HS-1199 and HS-1200 were employed for this study. General evaluations focusing on cell cycle were conducted in HT -29 human colon adenocarcinoma cell line (p53 mutant type). (omitted)

• Biomolecules & Therapeutics
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• v.23 no.3
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• pp.225-232
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• 2015

We identified a novel Akt signaling mechanism that mediates fucoidan-induced suppression of human colon cancer cell (HT29) proliferation and anticancer effects. Fucoidan treatment significantly inhibited growth, induced G1-phase-associated upregulation of p21WAF1 expression, and suppressed cyclin and cyclin-dependent kinase expression in HT29 colon cancer cells. Additionally, fucoidan treatment activated the Akt signaling pathway, which was inhibited by treatment with an Akt inhibitor. The inhibition of Akt activation reversed the fucoidan-induced decrease in cell proliferation, the induction of G1-phase-associated p21WAF1 expression, and the reduction in cell cycle regulatory protein expression. Intraperitoneal injection of fucoidan reduced tumor volume; this enhanced antitumor efficacy was associated with induction of apoptosis and decreased angiogenesis. These data suggest that the activation of Akt signaling is involved in the growth inhibition of colon cancer cells treated with fucoidan. Thus, fucoidan may serve as a potential therapeutic agent for colon cancer.

• The Korean Journal of Food And Nutrition
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• v.15 no.1
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• pp.23-28
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• 2002

The inhibitory effects of persimmon leaves on th e mutagenicity in spore rec assay and on the growth of HT-29 human colon cancer cells and AZ-521 human gastric cancer cells were studied. Methanol extract of persimmon leaves inhibited the mutagenicity induced fly N-methyl- N'-nitro-N-nitrosoguanidine(MNNG) in spore rec assay. The hexane, chloroform and ethylacetate fraction from the methanol extract exhibited strong antimutagenicity against MNNG in spore rec assay The methanol extract of persimmon leaves also revealed the inhibitory effects on the growth of HT-29 human colon cancer cells and AZ-521 human gastric cancer cells. Among the solvent extracted fraction from the methanol extract, the chloroform fraction was most effective and inhibited the growth of HT-29 and AZ-521 cells by 100 percent.

• YAKHAK HOEJI
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• v.53 no.4
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• pp.184-188
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• 2009

Fluorouracil (5-FU) is one of the most widely used chemotherapeutic drugs in the treatment of advanced colorectal cancer patients. Capsaicin (N-vanillyl-8-methyl-alpha-nonenamide), a spicy component of hot pepper, is a homovanillic acid derivative that preferentially induces cancer cells to undergo apoptosis. The purpose of the present study is to examine whether capsaicin enhances the anticancer effect of 5-fluorouracil in HT-29 human colon cancer cells by inducing apoptosis, and whether PPARgamma is involved in the capsaicin action in combination treatment with 5-FU. Treatment of the cells with either 5-FU or capsaicin alone for 48 h had little effect on the cell viability up to $50{\mu}M$ concentration, whereas co-treatment of the cells with capsaicin in the presence of 5-FU for 48 h significantly decreased the cell viability in a concentration-dependent manner. In addition, caspase-3 activity, a marker enzyme for apoptosis, was significantly increased by the combined treatment with 5-FU and capsaicin compared to the 5-FU or capsaicin alone treatment. Also, treatment with troglitazone, a peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) agonist, further enhanced the effect of the combination treatment on the cell viability and caspase-3 activity, and bisphenol A diglycidyl ether (BADGE), a $PPAR{\gamma}$ antagonist, blocked the effect of the combination treatment. These results suggest that the combination treatment of HT-29 cells with 5-FU and capsaicin induces apoptotic cell death at relatively low concentration than each drug alone, and the combination treatment may be associated with the $PPAR{\gamma}$ pathway activation.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6349-6355
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• 2012

Previous studies showed that Math1 homologous to human Hath1 can cause mouse goblet cells to differentiate. In this context it is important that the majority of colon cancers have few goblet cells. In the present study, the potential role of Hath1 in colon carcinogenesis was investigated. Sections of paraffin-embedded tissues were used to investigate the goblet cell population of normal colon mucosa, mucosa adjacent colon cancer and colon cancer samples from 48 patients. Hath1 and Muc2 expression in these samples were tested by immunohistochemistry, quantitative real-time reverse transcription -PCR and Western blotting. After the recombinant plasmid, pcDNA3.1(+)-Hath1 had been transfected into HT29 colon cancer cells, three clones were selected randomly to test the levels of Hath1 mRNA, Muc2 mRNA, Hath1, Muc2, cyclin D1 and p27 by quantitative real-time reverse transcription-PCR and Western blotting. Moreover, the proliferative ability of HT29 cells introduced with Hath1 was assessed by means of colony formation assay and xenografting. Expression of Hath1, Muc2, cyclin D1 and p27 in the xenograft tumors was also detected by Western blotting. No goblet cells were to be found in colon cancer and levels of Hath1 mRNA and Hath1, Muc2 mRNA and Muc2 were significantly down-regulated. Hath1 could decrease cyclin D1, increase p27 and Muc2 in HT29 cells and inhibit their proliferation. Hath1 may be an anti-oncogene in colon carcinogenesis.

• Food Engineering Progress
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• v.15 no.1
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• pp.64-69
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• 2011

The anticancer activity of Schizandra chinensis Baillon was investigated for the development of functional food resources. The antiproliferative activity of hot water extracts of Schizandra chinensis Baillon in human colon cancer cell line (HT-29) were identified using cell viability, morphology study, cell cycle and RT-PCR analyses. HT-29 cells were cultured in several concentrations (0, 1.0, 2.0, 4.0 mg/mL) of water extracts of Schizandra chinensis Baillon. In our study, colon cancer cell growth could be inhibited by hot water extracts of Schizandra chinensis Baillon in a dose-dependent manners. It was associated with morphological changes and apoptotic cell death with cell shrinking, chromatin condensation, apoptotic bodies and cell cycle analysis. These results suggest that Schizandra chinensis Baillon may inhibit the growth of human colon cancer cells by various apoptosis-aiding activities as well as apoptosis itself.

• Biomolecules & Therapeutics
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• v.19 no.2
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• pp.211-217
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• 2011

Panax ginseng CA Meyer, a herb from the Araliaceae, has traditionally been used as a medicinal plant in Asian countries. Ginseng extract fermented by ginsenoside-${\beta}$-glucosidase treatment is enriched in ginsenosides such as Rh2 and Rg3. Here we show that a fermented ginseng extract, BST204, has anti-proliferative and anti-invasive effects on HT-29 human colon cancer cells. Treatment of HT-29 cells with BST204 induced cell cycle arrest at $G_1$ phase without progression to apoptosis. This cell cycle arrest was accompanied by up-regulation of tumor suppressor proteins, p53 and p21$^{WAF1/Cip1}$, down-regulation of the cyclin-dependent kinase/cyclins, Cdk2, cyclin E, and cyclin D1 involved in $G_1$ or $G_1/S$ transition, and decrease in the phosphorylated form of retinoblastoma protein. In addition, BST204 suppressed the migration of HT-29 cells induced by 12-O-tetradecanoylphorbol-13-acetate, which correlated with the inhibition of metalloproteinase-9 activity and extracellular signal-regulated kinase activity. The effects of BST204 on the proliferation and the invasiveness of HT-29 cells were similar to those of Rh2. Taken together, the results suggest that fermentation of ginseng extract with ginsenoside-${\beta}$-glucosidase enhanced the anti-proliferative and the anti-invasive activity against human colon cancer cells and these anti-tumor effects of BST204 might be mediated in part by enriched Rh2.

• Journal of Nutrition and Health
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• v.33 no.1
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• pp.80-85
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• 2000

This study was undertaken to investigate the inhibitory effects of propolis on the in vitro proliferation of human colon(HT-29) and hepatoma(HepG2) cancer cell lines. The growth of the HT-29 and HepG2 cells was respectively inhibited by the administration of propolis in a concentration response-dependent manner. The distributions of HT-29 and HepG2 cells cultured in the medium containing propolis were shifted to the smaller sizes, and then HT-29 and HepG2 cells were shrunken under microscopic observations. The progression of cell cycle from G1 to S phase was significantly inhibited by propolis in the HT-29 and HepG2 cell lines, respectively. Those observations suggest that propolis has anticancer effect against some of cancer cell lines in vitro. (Korean J Nutrition 33(1) : 80-85, 2000)

• Journal of Life Science
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• v.7 no.3
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• pp.234-240
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• 1997

The anticarcingenic effect of methanol extracts from such cruciferous vegetables as cabbage, red cabbage, Korean cabbage, kale, cauliflower, broccoli, radish root, leafy radish, rape leaves and shepherd’s purse on the growth of human K-562 leukemia cells, MG-63 osteosarcoma cells, HT-29 colon cancer cells and AGS gastric cancer cells were studied. All of cruciferous vegetables inhibited more than 70% of the growth of K-52 leukemia cells and more than50% fo rhe growth fo AGS gastric cancer cells. Particularly, kale, broccoli and shepherd’s purse showed inhibition rates of 93.5%, 93,5% and 96.3% on the growth of AGS gastric cancer cells, respectively. In case of HT-29 colon cancer cells, the methanol extracts of cabbage, kale and shepherd’purse exhibited 82.4%, 72.15, 79.4% and 95.6% of inhibitory effects, respectively. The cabbage, kale, cauliflower and shepherd’s purse extracts also highly suppressed the proliferation of MG-63 cells. Generally the 10 cruciferous vegetable we studied strongly decreased the growth of various human cancer cells in vitro, however, kale and shepherd’s showed the most effective vegetable among them.