• Journal of Life Science
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• v.22 no.1
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• pp.55-61
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• 2012

Akt is known to play an important role in cell proliferation and differentiation, and is also over-expressed in several types of cancer cells. In this study, we explored the anti-proliferative effects of selenium in HT-29 colon cancer cells, mediated through effects on Akt and COX-2. Selenium treatments at different concentrations and for different durations inhibited proliferation of HT-29 colon cancer cells and increased apoptotic cell death. Selenium treatment decreased Akt phosphorylation and COX-2 expression. Treatment with LY294002 (an Akt inhibitor) decreased proliferation of HT-29 cells, while a combined treatment with LY294002 and selenium resulted in even further decreases in cell proliferation. Inactivation of Akt by Akt siRNA treatment abolished these inhibitory effects on cell growth. COX-2 expression decreased in Akt transfected cells compared to non-transfected cells. These results suggest that selenium induced both anti-proliferative and apoptotic effects by inhibiting Akt phosphorylation and COX-2 expression. Selenium treatment also appeared to induce synergistic anti-proliferative effects by inhibition of Akt in HT-29 colon cancer cells.

• 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 the Korean Society of Food Science and Nutrition
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• v.44 no.3
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• pp.338-346
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• 2015

This study was performed to elucidate the anti-proliferative and apoptotic mechanism of flavonoids in HT-29 human colon cancer cells. We investigated the anti-proliferative activity of flavonoids in HT-29 human colon cancer cells via cell viability assay (MTT assay), caspase-3 activity, RT-PCR, and western blotting. We cultured HT-29 cells in the presence of various flavonoids (apigenin, rutin, naringenin, and myricetin) at a concentration of $100{\mu}M$. In the MTT assay, naringenin showed the strongest effect on cell viability in HT-29 colon cancer cells. Caspase-3 activity, a marker of apoptosis, significantly increased upon naringenin treatment. For RT-PCR, myricetin significantly increased Bax protein levels, naringenin increased p53 protein levels, and rutin reduced expression of the anti-apoptotic protein Bcl-2. Western blotting of HT-29 colon cancer cells showed that myricetin increased cleaved caspase-3 protein levels, naringenin significantly increased poly (ADP-ribose) polymerase protein levels, and rutin increased E-cadherin protein levels. These results indicate that flavonoid exerts anticancer effects on human colon HT-29 cells through a caspase-dependent apoptotic pathway.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.12
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• pp.1827-1834
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• 2014

Colon cancer is the third highest cause of death in Korea. Known dietary causes of colon cancer include a diet rich in fat and red meat as well as inadequate intake of dietary fiber, fruits, and vegetables. Therefore, recent research has focused on the anticancer effects of natural products. Opuntia humifusa is a type of prickly pear that is known to contain biologically active compounds that can be used in the treatment of diabetes mellitus, arteriosclerosis, and hyperglycemia. The aim of this study was to determine whether or not O. humifusa extract affects proliferation, cell death, and DNA fragmentation in human carcinoma HT-29 cells. O. humifusa is rich in carbohydrates, minerals (Mg, K, and Ca), and total phenolics. HT-29 cells were treated with extracts of O. humifusa at concentrations of 0, 0.25, 0.5, 1, and 2 mg/mL for 24 or 48 hours. O. humifusa extracts inhibited HT-29 cell growth in a dose-dependent manner. Hoechst 33342/PI double staining and Comet assay were performed to observe changes in nuclei of cancer cells undergoing cell death. The results of both tests showed that O. humifusa extract induced cell shrinkage, DNA fragmentation, and chromatin condensation dose-dependently in HT-29 cells. The results of this study suggest that O. humifusa extract inhibits the growth of HT-29 via induction of DNA fragmentation and chromatin condensation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.2
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• pp.155-159
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• 2012

The purpose of this study was to investigate the anti-cancer effects of Sophorae Radix and the effects of 5-Fluorouracil (5-FU) in human colorectal adenocarcinoma cells (HT-29). We used human colorectal adenocarcinoma cell line, HT-29 cells. We examined cell death by MTT assay and caspase 3 assay with Sophorae Radix. To examine the inhibitory effects of Sophorae Radix, cell cycle (sub G1) analysis was done the HT-29 cells after three days with Sophorae Radix. The reversibility of Sophorae Radix was examined on one day to five days treatment with $150{\mu}g$ Sophorae Radix. Sophorae Radix inhibited the growth of HT-29 cells in a dose-dependent fashion. Also we showed that Sophorae Radix induced apoptosis in HT-29 cells by MTT assay, caspase 3 assay and sub-G1 analysis. Sophorae Radix combined with 5-FU markedly inhibited the growth of HT-29 cells compared to Sophorae Radix or 5-FU alone. After 3 days treatment of HT-29 cells with Sophorae Radix, the fraction of cells in sub-G1 phase was much higher than that of the control group. Our findings provide insight into unraveling the effects of Sophorae Radix in human colorectal adenocarcinoma cells and developing therapeutic agents against colorectal cancer.

• Journal of Nutrition and Health
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• v.34 no.2
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• pp.150-157
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• 2001

Intestinal absorption of dietary taurine is one of the regulatory component maintaining taurine homeostasis along with renal reabsorption, bile acid conjugation and secretion, and de nobo synthesis of taurine in mammals. Recent observations of decreased enterocytic levels of taurine in response to trauma, infection and surgical insults, postulate the possibility that intestinal taurine absorption might be impaired in such stressed conditions. The aim of the present study was to evaluate changes in enterocytic taurine transporter activity using the human intestinal colon carcinoma cell line, HT-29, in various stress-induced conditions. Pretreatment of the HT-29 cells with dexamethasone, a stress hormone(0.1,1,10 or 100$\mu$M) for 3 hrs, or with E coli heat-stable enterotoxin(10, 100, or 200nM) for 30 minutes in order to induce the condition of enterotoxigenic infection did not influence taurine uptake as compared to the value found in control cells. In contrast, pretreatment of the cells with cholera toxin(10, 100, 500, or 1000ng/ml)for 3hr or 24hr significantly decreased taurine uptake by HT-29 cells to 40~50% of the value found in untreated control cells. Kinetic studies of the taurine transporter activity were conducted in control and cholera toxin treated HT-29 cells with varying taurine concentrations(2~60$\mu$M) in the uptake medium. Pretreatment of the cells with cholera toxin(100ng/ml) for 3hr did not influence the Vmax, but resulted in a 55% increase in the Michaelis-Menten constant(Km) of the taurine transporter compared to those in control cells. These results suggest that cholera toxin-induced reduction in taurine transporter activity in HT-29 cells is associated with decreased affinity of the taurine transporter without altering the amount of transporter protein. Intestinal taurine absorption appears to be reduced in the condition of water-borne diseases caused by bacteria such as V. cholerae. This might influence the taurine status of infants and young children more readily, an age group in which the prevalence of intestinal infection is high and the role of intestinal absorption is crucial for maintaining the body taurine pool. (Korean J Nutrition 34(2) : 150-157, 2001)

• KSBB Journal
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• v.27 no.5
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• pp.289-294
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• 2012

Resveratrol, natural polyphenol in grapes and red wine, is known to have the anti-proliferatory and anti-angiogenic effects in various cancer cells. In this study, we have investigated the effects of resveratrol in HT-29 colon cancer cells. Treatment of resveratrol in different concentrations and time inhibited proliferation of HT-29 colon cancer cells. We explored the effects of resveratrol on HT-29 colon cancer cell motility using a wound healing assay. In the absence of the resveratrol, the HT-29 cells are migrated along the edges of the wound and showed a large-scale migration, whereas dose- and time-dependent inhibition of cell flattening and spreading was observed in the presence of resveratrol. Resveratrol inhibited MMP-9 in a dose- and time-dependent on HT-29 colon cancer cells by Western blotting. In addition, resveratrol increased AMPK activity and decreased COX-2, VASP and VEGF expression. Treatment of compound C inhibited AMPK activity, however, the expression of VASP and COX-2 increased thus, COX-2 and VASP are modulated by AMPK. However treatment of celecoxib could not control AMPK activity but decreased VEGF expression. We suggest that resveratrol inhibits cell proliferation and migration through activation of AMPK and decreased COX-2, VASP and VEGF expression in HT-29 colon cancer cells.

• 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.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.

• Archives of Pharmacal Research
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• v.27 no.12
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• pp.1253-1257
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• 2004

6-Methoxydihydrosanguinarine (6ME), a benzophenanthridine alkaloid derived from the methanol extracts of Hylomecon hylomeconoides, showed a dose-dependent effect at 1-10 ${\mu}M$ on causing apoptotic cell death in HT29 colon carcinoma cells $(IC_{50} = 5.0{\pm}0.2 {\mu}M)$. Treatment of HT-29 cells with 6ME resulted in the formation of internucleosomal DNA fragmentation. Treatment of the cells with 6ME caused activation of caspase-3, -8 and 9 protease and subsequent proteolytic cleavage of poly(ADP-ribose)polymerase. 6ME increased the expression of p53 and Bax and decreased the expression of Bid. These results indicate that p53 and proapoptotic Bcl-2 family proteins might participate in the antiproliferative activity of 6ME in HT29 cells.