• Parasites, Hosts and Diseases
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• v.51 no.1
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• pp.61-68
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• 2013

Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoebainduced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica.

• The Journal of Dong Guk Oriental Medicine
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• v.11
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• pp.52-57
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• 2008

Objectives. In this study, we investigate that methanol extract of Euphorbiae lathyridis Semen contributes to growth inhibitory effect on the HT-29 human colon cancer cells. Methods. Euphorbiae lathyridis Semen (ELS) was extracted with 80% methanol. HT-29 cells were treated with different concentrations of ELS extract for 24-72 hrs. Growth inhibitory effect was determined by MTT assay. Cell apoptosis was determined by surveying caspases cascades activation using Western blot. Cell cycle arrest was analyzed by flow cytometry with PI staining. Results. Exposure to ELS extract showed in inhibitory effects on HT-29 cell growth as a dose-dependent manner. Cell growth inhibition by ELS extract was related with induction of cell apoptosis with DNA fragmentation through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion. ELS extract significantly inhibited cell growth and induced cell apoptosis in HT-29 human colon cancer cells, therefore, These results suggest that ELS extract can be used as chemoprevention agent of colon cancers.

• 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)

• Food Science and Biotechnology
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• v.14 no.6
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• pp.866-870
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• 2005

The 14 lactic acid bacteria (LAB) have been evaluated to determine the binding capacity to HT29 cell and Aflatoxin $B_1$ ($AFB_1$). The interaction of LAB to HT29 cells has been further investigated to identify the possibility of competing the binding sites with $AFB_1$. Of 14 LAB strains, Lactobacillus casei KCTC 3260 demonstrated the higher adhesiveness to HT29 and $AFB_1$ with the rate of 19.6% and 46.3%, respectively. In competitive analysis for binding sites, the adhesion of L. casei KCTC 3260 to HT29 cells was reduced with 100 nmol $AFB_1$ by 31.2%. The protoplast of L. casei KCTC 3260 showed no binding capacity to HT29 cells with increment of $AFB_1$ concentration, indicating that cell wall components might serve as a critical factor for the binding. To discriminate the major component influencing on L. casei KCTC 3260 binding to HT29 cells and $AFB_1$, four different pre-treatments (lipase, pronase E, sodium m-periodate, and urea) were employed. Of those, sodium m-periodate treatment caused the lower adhesion of L. casei KCTC 3260 to HT29 cells with the increment of $AFB_1$ concentration. These results indicated that carbohydrate moiety on the cell wall of L. casei KCTC 3260 might be the most critical component in binding to both HT29 cells and $AFB_1$.

• Korean Journal of Pharmacognosy
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• v.42 no.3
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• pp.282-287
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• 2011

This study was presented to the anti-cancer activity from different fraction of Zanthoxylum schnifolium fruits. The values for human colon cancer cell(HT-29) survival rate of 0.3 mg/mL of 70% EtOH and 70% MeOH ethyl acetate fraction extracts were 7.62${\pm}$0.173%, 7.66${\pm}$0.037%, respectively. It was shown that human colon cancer cell(HT-29) survival rate was in a dose-dependent manner. The percentages of cells were increased in the sub-G0 and G0/G1 phase region, meaning that cell proliferation was decreased. The RT-PCR demonstrated that 70% EtOH and 70% MeOH ethyl acetate fraction extracts were down-regulated the expression of Bcl-2 and survivin genes in HT-29 cells. We examined that 70% EtOH and 70% MeOH ethyl acetate fraction extracts anti-cancer activities initiated through ROS generation suggesting that HT-29 cells treated with ethyl acetate fraction extracts induced ROS generation. Our results revealed that the Zanthoxylum schnifolium fruit may expect for anti-cancer activities in HT-29 cells.

• The Korea Journal of Herbology
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• v.22 no.2
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• pp.65-72
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• 2007

Objectives : In this study, we investigate that Euphorbiae lathyridis Semen extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Euphorbiae lathyridis Semen was extracted from the Semen of the plant using 80% Methanol. The Euphorbiae lathyridis Semen extract was treated to different concentrations for 24 hr, 4Shr or 72hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Westem blot. Results : Exposure to Euphorbiae lathyridis Semen extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Euphorbiae lathyridis Semen extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Euphorbiae lathyridis Semen extract induces DNA fragmentation in HT-29 cells. Furthermore, Euphorbiae lathyridis Semen extract induces cell apoptosis through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion : Euphorbiae lathyridis Semen extract induces apoptosis in human colon cancer cells, therefore, we suggest that Euphorbiae lathyridis Semen extract can be used as a novel class of anti-cancer drugs.

• 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 Nutrition and Health
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• v.33 no.6
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• pp.660-667
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• 2000

Previous studies on the effect of age on intestinal taurine transport in animals have invariably shown a decline in the activity of the transport system with increasing age. In the present study changes in taurine transporter activity were observed during cell differentiation in the human colon carcinoma cell line HT-29 This cell line exhibits various enterocytic characteristics when differentiated and therefore has frequently been used to study the characteristcs and regulation of nutrient and drug absorption in the small intestine at the cellular level. Pre-treatment of the cells with $\beta$-alanine(10mM) reduced the taurine transport activity to 33% of the value for the control cells(p<0.05) which implies that taurine and $\beta$-alanine share a common $\beta$-amino acid transport system for their celluar uptake in the HI-29 was continued until 21 days post seeding. Kinetic studies of the taurine transporter were conducted in the HT-29 cell line with varying taurine concentration(5-60$\mu$M) in the uptake medium Both Vmax and the Michaelis-Menten constant(Km) of taurine transporter were decreased as differentiation of the HT-29 cell line was progressed ; Vmax of the taurine transporter in cells incubated for 4, 14 and 21 days post seeding was 2.79$\pm$3.4m 16.89$\pm$1.74, and 0.85$\pm$0.08 and 0.32$\pm$0.01nmol.mg protein-1 .30min-1 respectively(p<0.001) and Km was 42.3$\pm$3.4, 16.89$\pm$1.74, and 11.2$\pm$3.0$\mu$M respectively (p<0.01) These results indicate that the activity of sodium dependent active taurine transport system in the HT-29 cell line is decreased as confluent cells are differentiated. This phenomenon in cell culture system corresponds well with the earlier observation of lower intestinal taurine transport activity in suckling rats compared to that in adult animals although direct relationship of cell differentiation with in vivo aging process needs further verification.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1871-1877
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• 2014

Enhancing of radioresponsiveness of tumors by using radiosensitizers is a promising approach to increase the efficacy of radiation therapy. Recently, the ethanolic extract of the medicinal plant, Derris scandens Benth has been identified as a potent radiosensitizer of human colon cancer HT29 cells. However, cell death mechanisms underlying radiosensitization activity of D scandens extract have not been identified. Here, we show that treatment of HT-29 cells with D scandens extract in combination with gamma irradiation synergistically sensitizes HT-29 cells to cell lethality by apoptosis and mitotic catastrophe. Furthermore, the extract was found to decrease Erk1/2 activation. These findings suggest that D scandens extract mediates radiosensitization via at least two distinct modes of cell death and silences pro-survival signaling in HT-29 cells.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.51-58
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• 2006

Objectives : In this study, we investigate that Ulmi cortex extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Ulmi cortex was extracted from the leaves of the plant using water. The Ulmi cortex extract was treated to different concentrations for 24 hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell cycle inhibition was confirmed by kinases assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Western blot. Results : Exposure to Ulmi cortex extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Ulmi cortex extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Ulmi cortex extract induces G1-cell cycle arrest and DNA fragmentation in HT-29 cells. Furthermore, Ulmi cortex extract induces cell apoptosis through the activation of caspases-3 and PARP cleavage. Conclusion : Ulmi cortex extract induces apoptosis in human colon cancer cells, therefore, we suggest that Ulmi cortex extract can be used as a novel class of anti-cancer drugs.