• Preventive Nutrition and Food Science
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• v.5 no.2
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• pp.114-118
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• 2000

The inhibitory effects of doenjang extracts and linoleic acid(LA) which was identified as one of the active compounds in doenjang on the growth of human cancer cells were studied, comparing to the actions on normal cells. Methanol extract and hexane fraction from doenjang exhibited the strong growth inhibitory effect on HT-29 human colon carcinoma cells. Inhibitory effects of chloroform, ethyl acetate, butanol and aqueous fractions on the cancer cells were observed, moderately or weakly. When cell counts of SNU-C$_1$human colon carcinoma cells were determined daily for 6 days, the inhibitory effect of hexane fraction on this cell line was higher than that of the methanol extract from doenjang. LA completely suppressed the growth of SNU-C$_1$cells after 4 days, while conjugated linoleic acid(CLA) resulted in 98% inhibition after 6 days. With the addition of LA and other free fatty acids such as stearic acid, oleic acid, linolenic acid and ${\gamma}$-linolenic acid (${\gamma}$-LnA) to the culture system, the growth of HT-29 cells and SNU-C$_1$cells was greatly suppressed after 6 days. Inhibitory effects of LA ${\gamma}$-LnA on the growth of these cells were stronger than other fatty acids. On the growth of AZ-521 human gastric carcinoma cells, LA and CLA completely cuppressed the growth of the cells after 4 days and 3 days, respectively. At the level of 0.001%~0.01% of LA, there was no cytotoxic effect on normal rat kidney cells and normal intestine human cells. These results showed that LA, a major active compound of doenjang, had strong inhibitory effects on the growth of human cancer cells without damaging normal 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.24 no.6
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• pp.604-609
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• 2016

5-fluorouracil (5-FU) is a chemotherapeutic agent commonly used for treatment of solid tumors, including colorectal cancer. However, chemoresistance against 5-fluorouracil (5-FU) often limits its success for chemotherapy and, therefore, finding out appropriate adjuvant(s) that might overcome chemoresistance against 5-FU bears a significant importance. In the present study, we have found that ${\alpha}$-mangostin can sensitize 5-FU-resistant SNUC5/5-FUR colon cancer cells to apoptosis. Exposure of ${\alpha}$-mangostin induced significant DNA damages and increased the intracellular 8-hydroxyguanosine (8-OH-G) and 4-hydroxynonenal (4-HNE) levels in SNUC5 and SNUC5/5-FUR cells. Western blot analysis illustrated that ${\alpha}$-mangostin-induced apoptosis was mediated by the activation of the extrinsic and intrinsic pathways in SNUC5/5-FUR cells. In particular, we observed that Fas receptor (FasR) level was lower in SNUC5/5-FUR cells, compared with SNUC5 cells and that silencing FasR attenuated ${\alpha}$-mangostin-mediated apoptosis in SNUC5/5-FUR cells. Together, our study illustrates that ${\alpha}$-mangostin might be an efficient apoptosis sensitizer that can overcome chemoresistance against 5-FU by activating apoptosis pathway.

• Archives of Pharmacal Research
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• v.14 no.3
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• pp.207-216
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• 1991

Pseudixus japonicus agglutinin (PJA) was isolated. And its characteristics were compared with those of concanavalin A (Con A). PJA is a glycopritein composed of 49.3% carbohydrate and 50.7% protein which had relatively high percentages of glutamic acid, aspartic acid and phenylalanine residues. The hemagglutinating activity of PJA was approximately one-eighth of that of Con A when tested with mouse crythrocytes. PJA failed to simulate the proliferation or transformation of human and mouse lymphocytes in contratst to Con A. PJA and Con A showed cytotoxicities against SNU-1 (human stomach cancer cells), SNU-CI (human colon cancer cells) and mouse Sarcoma 180 cells when tested by 3-(4, 5-dimethyl thiazol-2-yl)2. 5-diphenyl tetrazolium bromide (MIT) colorimetric assay. The antitumor activity of the lectin in vivo was also tested in Sarcoma 180 bearing mice. There was no significant difference in prologation of lifc span of the mice after the treatment with PJA and Con A for 10 consecutive days.

• Preventive Nutrition and Food Science
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• v.13 no.3
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• pp.157-165
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• 2008

Cancer-preventive effects of ethanol extract of elm tree root (EEE) were investigated. In the in vitro cytotoxicity assay, colon cancer cells were incubated with a chloroform fraction of EEE (CF-EEE). CF-EEE significantly inhibited the proliferation of cells and induced apoptotic cell death in a dose-dependent manner. For the assessment of chemopreventive efficacy in vivo, male F344 rats were fed with EEE (0.5 or 1%) in diet for 8 weeks, and were subcutaneously injected with 1,2-dimethylhydrazine (DMH) to induce colonic aberrant crypt foci (ACF). EEE (0.5 and 1%) significantly decreased both the numbers of AC (1191.1/colon) and ACF (529.3/colon) induced by DMH. In addition, in the Western blot analysis on the colonic mucosa, administration of EEE triggered expression of caspase-3, a key factor of an apoptotic cascade. These results suggest that extract of elm tree root may have potential chemopreventive principles that lead to apoptosis of cancer cells, and thereby suppress colorectal carcinogenesis during the initiation stage.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.9
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• pp.1115-1120
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• 2006

The effect of cinnamon ethanol extract (CN) on HT-29 cancer cell line has been examined. CN inhibited the growth of HT-29 colon cancer cells in a concentration and time dependent manner but not the growth of CCD-112CoN normal colon cells. And CN markedly inhibited the production of $PGE_2$ and cGMP as well as the mRNA expression of COX-2. These data suggest that non toxic concentration of CN has a significant inhibition effect on the growth of HT-29 cells, probably through the inhibition of $PGE_2$ production via COX-2 inhibition, and may have value as a safe chemopreventive agent for colon cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4263-4266
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• 2012

Colorectal cancer has become a major disease threatening human health. To establish animal models that exhibit the characteristics of human colorectal cancer will not only help to study the mechanisms underlying the genesis and development effectively, but also provide ideal carriers for the screening of medicines and examining their therapeutic effects. In this study, we established a stable, colon cancer nude mouse model highly expressing green fluorescent protein (GFP) for spontaneous metastasis after surgical orthotopic implantation (SOI). GFP-labeled colon cancer models for metastasis after SOI were successfully established in all of 15 nude mice and there were no surgery-related complications or deaths. In week 3, primary tumors expressing GFP were observed in all model animals under fluoroscopy and two metastatic tumors were monitored by fluorescent imaging at the same time. The tumor volumes progressively increased with time. Seven out of 15 tumor transplanted mice died and the major causes of death were intestinal obstruction and cachexia resulting from malignant tumor growth. Eight model animals survived at the end of the experiment, 6 of which had metastases (6 cases to mesenteric lymph nodes, 4 hepatic, 2 pancreatic and 1 mediastinal lymph node). Our results indicate that our GFP-labeled colon cancer orthotopic transplantation model is useful with a high success rate; the transplanted tumors exhibit similar biological properties to human colorectal cancer, and can be used for real-time, in vivo, non-invasive and dynamic observation and analysis of the growth and metastasis of tumor cells.

• 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.

• Journal of Digestive Cancer Research
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• v.6 no.1
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• pp.11-15
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• 2018

Chemotherapy and surgical resection are the mainstay of cancer treatment. Particularly for chemotherapy, although it is effective method to care, sometimes cure various cancers, there are many different status of cancer not being controlled by chemotherapy such as recurrence and resistance to chemotherapy. In order to overcome those difficulties during cancer therapy, immunotherapy targeting immune cells and immune associated factors to enhance cancer immunity has been highlighted. Innate immunity plays important roles on initial stage of cancer immunity that are detecting, killing cancer cells and initiating adaptive immunity for cancer. So many basic and clinical studies to manage innate immunity for cancer therapy have been going on, and most of them were to stimulate innate immune cells including dendritic cell, macrophage, monocyte, and natural killer cell in various ways. They showed promising results but still there are many things to be resolved before clinical application. Herein, I review the role of innate immune cells and therapeutic trials for colorectal cancer.

• Food Science and Biotechnology
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• v.18 no.3
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• pp.749-754
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• 2009

The polysaccharide (BB-pol) extracted from Bifidobacterium bifidum BGN4 showed growth inhibitory effects on several colon cancer cell lines such as HT-29 and HCT-116. To increase the yield of polysaccharide, B. bifidum BGN4 was cultured in various culture media with different compositions. When B. bifidum BGN4 was cultured in modified MRS broth containing phytic acid, the cells showed increased branch formation and enlarged morphology. The content of total carbohydrate and the ability of adhesion to intestinal epithelial cells were also increased by phytic acid. The polysaccharide obtained from the cells grown in the presence of phytic acid inhibited the proliferation of cancer cell lines such as HT-29 and MCF-7 cells but not normal colon cell line, FHC. Taken together, Bifidobacterium grown in the presence of phytic acid may confer enhanced beneficial function for the host.