• 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.

• Journal of Life Science
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• v.25 no.5
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• pp.515-522
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• 2015

Treculia africana Decne, a breadfruit species, is native to many parts of West and Tropical Africa. The breadfruit belongs to the family Moraceae and is one of the four members of the genera Treculia. The crude extract of T. africana has been used in folk medicine as an anti-inflammatory agent for various ailments, such as whooping cough. In this study, we evaluated the anti-oxidative and anti-cancer activities of the methanol extract of T. africana Decne (META) and the molecular mechanisms of its anti-cancer effects in human colon carcinoma HT29 cells. The META exhibited anti-oxidative activity through a DPPH radical scavenging capacity and inhibited cell growth in a dose-dependent manner in HT29 cells. META treatment induced apoptosis of HT29 cells, showing an increase in the percentage of both SubG1 cells and Annexin V-positive cells and the formation of apoptotic bodies in a dose-dependent manner. META-mediated apoptosis was associated with the up-regulation of the death receptor FAS and Bax and a decrease in the Bcl-2 expression. META-treated HT29 cells also showed the release of cytochrome c from the mitochondria into the cytosol, activation of caspase-3, caspase-8, and caspase-9, and proteolytic cleavage of poly ADP-ribose polymerase (PARP). These findings suggest META may exert an anti-cancer effect in HT29 cells by inducing apoptosis through both intrinsic and extrinsic pathways.

• Journal of Life Science
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• v.24 no.9
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• pp.1012-1018
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• 2014

Sasa quelpaertensis Nakai (Korean name, Jeju-Joritdae) is one of the most abundant plants on Mt. Halla, Jeju Island, and it has long been used in traditional medicines. Recent studies have reported it as possessing various beneficial functions, including anti-inflammatory, anti-diabetic, anti-hypertension, anti-gastritis, anti-oxidant, and anti-cancer effects. However, the molecular mechanisms of its anti-cancer activity have not been clearly elucidated. In this study, we investigated the anti-cancer effects and mechanism of S. quelpaertensis on human colon cancer HT-29 cells. Cell growth inhibition by S. quelpaertensis was determined by MTT assay. Apoptosis was performed by DNA fragmentation, flow cytometry with propidium iodide staining (PI), and reverse transcription-polymerase chain reaction (RT-PCR) to confirm the anti-apoptotic factors, such as inhibitor of apoptosis (IAP) family members. $NO^{\bullet}$ production was determined by Griess assay. S. quelpaertensis treatment resulted in the time- and dose-dependent inhibition of the cell viability of HT-29 cells by inducing apoptosis, as evidenced by the accumulation of the sub-G1 cell population stained by PI, as well as the ladder-like DNA fragmentation in a dose-dependent manner. S. quelpaertensis-inducing apoptosis was accompanied by the induction of S cell cycle arrests, increasing $NO^{\bullet}$ concentrations, and the down-regulation of IAPs, including X-chromosome-linked IAP (XIAP), cellular IAP-1 (cIAP-1), cIAP-2, and survivin. Taken together, these findings have important implications for future clinical developments of S. quelpaertensis in colon cancer treatment.

• Korean Journal of Food Science and Technology
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• v.49 no.3
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• pp.242-251
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• 2017

The purpose of this study was to investigate the anti-proliferative effect of methanolic extracts from Citrus junos (yuja) seeds and yuja seed oils against HT-29 human colon cancer cells and to identify the key compounds responsible for this effect. Extracts from yuja seeds, yuja seed oil prepared using hexane, and cold-pressed yuja seed oil were prepared using 60% methanol (ES, EHO, and ECO, respectively). The key compounds in the extracts were determined using HPLC-MS. Among the extracts, EHO and ECO inhibited proliferation of HT-29 cells. EHO and ECO were fractionated using preparative LC and the bioactive compounds were determined. Five of the fractions showed a significant anti-proliferative effect and the main compounds in the fractions were isopimpinellin, bergapten, and ichangensin. These compounds showed anti-proliferative effects on HT-29 cells when treated individually, and ichangensin showed the highest anti-proliferative activity. These results suggest that these compounds may be responsible for the anti-cancer effect of EHO and ECO.

• Applied Chemistry for Engineering
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• v.25 no.4
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• pp.363-367
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• 2014

In this study, the dietary fiber contents of Mozuku (Cladosiphon novae-caledoniae kylin) residue and the extraction condition (HCl, $H_2SO_4$, NaOH, $Na_2CO_3$, $Na_2EDTA$) of the dietary fiber was investigated. We examined that the contents of the total polyphenols and flavonoids in the dietary fiber from Mozuku residue, and the potent anti-cancer effect was also tested through the growth inhibition in human colon cancer cells (HT-29) in vitro. It was effective to extract soluble dietary fiber with 1.5% $Na_2EDTA$ and 0.05 N HCl in Mozuku residue. The extraction time and temperature affected the yields of soluble dietary fiber. The contents of the total polyphenols and flavonoids in the dietary fiber from Mozuku residue were the highest in 1% NaOH extract (Total polyphenols $34.4{\pm}0.055$ mg gallic acid/g dry basis, total flavonoids $34.7{\pm}0.023$ mg naringin/g extract dry basis). In DPPH radical scavenging activity, 1% NaOH extract showed the most potent antioxidant activity. In the result of viability in human colon cancer cells, growth inhibition was observed in D.W., 0.05 N HCl, and 0.5% $Na_2CO_3$ extracts in a dose-dependent manner. These results demonstrated that soluble dietary fiber from Mozuku residue significant antioxidant activity and anticancer in human colon cancer.

• Journal of the Korean Society of Food Culture
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• v.24 no.6
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• pp.749-755
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• 2009

We investigated the chemical components of red onion powder dried using the low temperature vacuum method and the inhibitory effects of solvent extracts of the dried red onion powder on the growth of HT-1080 human fibrosarcoma and HT-29 human colon cancer cells and $H_2O_2$-induced oxidative stress. The moisture content of the dried red onion powder was 17.95%, while the vitamin C content was 96 mg/100 g and the total phenols content was 39.1 mg/mL. The inhibitory effects of acetone with methylene chloride (A+M) and methanol (MeOH) extracts of the red onion powder on the growth of HT-1080 and HT-29 cancer cells increased in a dose dependent manner (p<0.05). The inhibitory effect was greater on the growth of HT-29 cells, while the A+M extracts had a higher inhibitory effect than the MeOH extracts. Treatment with the hexane, 85% aq. methanol, butanol and water fractions of the extract led to significant inhibition of the growth of both cancer cell lines (p<0.05). Among the fractions, the hexane and 85% aq. methanol fractions showed a greater inhibitory effect. To determine the protective effect on $H_2O_2$-induced oxidative stress, a DCFH-DA (dichlorodihydrofluorescin diacetate) assay was conducted. All fractions, including the crude extracts of dried red onion, appeared to lead to a significant reduction in the levels of intracellular reactive oxygen species (ROS), and these reductions occurred in a dose dependent fashion (p<0.05). Among the fractions, the 85% methanol fraction showed the greatest protective effect on the production of lipid peroxides.

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.144-149
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• 2008

Despite versatile activity (cancericidal, antimicrobial, hypoxia inducible factor (HIF) inhibition, immune deactivation of DNA bis-intercalation agent, echinomycin, its specific mechanism has been elusive. Of these novel mechanisms, we reported that using human colon cancer cells (HT-29), apoptotic machinery induced by echinomycin might be dependent of caspase-3 pathway. Despite a partial enlightenment of prototypic signal path triggered by echinomycin, the role of Bcl-2 in this signaling pathway is unclear. To address this issue, we explored whether or not echinomycin would overcome the anti-apoptotic impact of Bcl-2 in HT-29 cells by the controlled Bcl-2 overexpression. Prior to this proof, we confirmed that echinomycin induces mitochondrial depolarization, then triggering the mitochondrial pathway of apoptosis with an involvement of upstream cas-pases-3. Transiently transfection with inactive Bax-DNA failed to prevent echinomycin-induced apoptosis in HT-29 cells. To dissect the role of Bcl-2 in echinomycin-induced apoptosis, HT-29 cells were transiently transfected with Bcl-2 DNA for overexpression and then treated with echinomycin for 24h. Combined analyses of DNA fragmentation and flow cytometric analysis clearly verified that echinomycin-induced apoptosis was drastically attenuated by Bcl-2 overexpression, whereas a control vector rarely affected echinomycin-induced apoptosis. Collectively, these data verify that Bcl-2 regulates echinomycin-induced apoptosis in HT-29 cells. To my knowledge, this is the first evidence that of diverse, structured minor groove binders (MGB), the prototypic echinomycin might control the apoptotic signaling via Bcl-2-mitochondrial pathway.

• Journal of Ginseng Research
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• v.10 no.2
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• pp.141-150
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• 1986

This study was attempted to screen the cytotoxic activity of petroleum ether ex- tract from panax ginseng root against human colon cancer cells. Two extracts of panax ginseng root, crude and partially purified, were used for this experiment. The crude extract was prepared by extraction with petroleum ether using Soxhlet aparatus for 12 to 15 hours from panax ginseng and the extract was partially purified by silicic acid column with mixture of petroleum ether: ethyl ether (70 : 30, v/v). Three species of human colon cancer cells, HRT-18, HCT-48 and HT-29, were maintained in DMEM (Dulbecco's modified Eagle medium), and the cells were cultured in DMEM containing serial concentration of the crude or partially purified fraction to observe the cytotoxic activity of the both extracts. The effects of incubation time and concentration of the both extracts in culture medium against the growth of the each cancer cell were determined. The results obtained are summarized as follows: 1. The doubling times of the HRT-18, HCT-48 and HT-29 cells were about 20, 24 and 22 hours, respectively. 2, The inhibitory effects of the crude extract on the growth of cancer cells were increased according to the rise of concentration of the extract and incubation time. 3. The inhibitory effect of partially purified fraction on the growth of HRT-18 cell was about 4 times stronger than that of the crude extract under same experimental condition. 4 The inhibitory effects of the crude and purified fraction on the growth of each cancer cell were shown difference by the kind of the cancer cell. In view of the above results, it could be said that the petroleum ether extract of panax ginseng root inhibited the division of the human colon cancer cell, in vitro.

• 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.

• Journal of Nutrition and Health
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• v.55 no.1
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• pp.47-58
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• 2022

Purpose: Obesity and a high-fat diet (HFD) are risk factors for colorectal cancer. We have previously shown that luteolin (LUT) supplementation in HFD-fed mice markedly inhibits tumor development in chemically induced colon carcinogenesis. In this study, we evaluated the anticancer effect of LUT in the inhibition of cell proliferation in HFD-fed obese mice and HT-29 human colorectal adenocarcinoma cells grown in an adipocyte-derived medium. Methods: C57BL/6 mice were fed a normal diet (ND, 11.69% fat out of total calories consumed, n = 10), HFD (40% fat out of total calories consumed, n = 10), HFD with 0.0025% LUT (n = 10), and HFD with 0.005% LUT (n = 10) and were subjected to azoxymethane-dextran sulfate sodium chemical colon carcinogenesis. All mice were fed the experimental diet for 11 weeks. 3T3-L1 preadipocytes and HT-29 cells were treated with various doses of LUT in an adipocyte-conditioned medium (Ad-CM). Results: The weekly body weight changes in the LUT groups were similar to those in the HFD group; however, the survival rates of the LUT group were higher than those of the HFD group. Impaired crypt integrity of the colonic mucosa in the HFD group was observed to be restored in the LUT group. The colonic expression of proliferating cell nuclear antigen and insulin-like growth factor 1 (IGF-1) receptors were suppressed by the LUT supplementation in the HFD-fed mice. The LUT treatment (10, 20, and 40 µM) inhibited the proliferation and migration of HT-29 cells cultured in Ad-CM in a dose-dependent manner, as well as the differentiation of 3T3-L1 preadipocytes. Conclusion: These results suggest that the anticancer effect of LUT is probably due to the inhibition of IGF-1 signaling and adipogenesis-related cell proliferation in colon cancer cells.