• The Korean Journal of Food And Nutrition
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• v.35 no.6
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• pp.464-472
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• 2022

The present study was designed to investigate the antiproliferative activity and molecular mechanisms of Bibimbap in HT-29 human colorectal adenocarcinoma cells. Bibimbap extract inhibited the proliferation of HT-29 cells by 50% at a concentration of 10.1±0.17 mg/mL for 48 h. The population of live cells decreased slightly, and the morphology changed with a reduction in cell volume (pyknosis) with Bibimbap. Treatment with 5 mg/mL of Bibimbap resulted in slight cell shrinkage. Furthermore, as the Bibimbap dose increased to 10 mg/mL, these characteristics were more evident, and HT-29 cells exhibited partial detachment by staining with the DNA-binding dye Hoechst 33342. Flow cytometric analysis by Annexin V and PI double staining showed that Bibimbap increased the levels of apoptosis. Analysis of the mechanism of these events showed that Bibimbap-treated cells exhibited a mitochondria-dependent apoptotic pathway through the modulation of caspase-3, caspase-8, caspase-9, and poly-ADP ribose polymerase, as well as Bax and Bcl-2 expression in dose- and time-dependent manners. Consequently, Bibimbap exerts a significant antiproliferative effect on HT-29 human colorectal adenocarcinoma 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.

• 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.

• 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.

• 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 Microbiology and Biotechnology
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• v.17 no.12
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• pp.2042-2045
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• 2007

The effect of chitosan oligosaccharide (COS, 1 kDa${\gamma}$, 10 ng/ml IL-$1{\alpha}$, and 25 ng/ml TNF-${\alpha}$) in HT-29 cells. Inducible nitric oxide synthase (iNOS) expression induced by these cytokines was inhibited by COS. COS pretreatment inhibited the invasiveness of cytokines-treated HT-29 cells through Matrigel-coated membrane in a dose-dependent manner. COS also inhibited cytokines-induced matrix metalloproteinase (MMP)-2 activity. This study shows that proinflammatory cytokines induce NO production, iNOS expression, and invasiveness of human colorectal adenocarcinoma HT-29 cells. COS pretreatment inhibited cytokines-mediated NO production, iNOS expression, and invasiveness of HT-29 cells. These results provide sufficient information for the further development of COS as an antitumor metastatic agent for the treatment of colon cancer.

• 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)

• 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 the Korean Society of Food Science and Nutrition
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• v.28 no.6
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• pp.1326-1331
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• 1999

In vitro anticancer effect of Chinese cabbage kimchi fractions was investigated by using human cancer cells, AGS human gastric adenocarcinoma cells and HT 29 human colon adenocarcinoma cells. The Chinese cabbage kimchi(fermented for 4 days at 15oC) was fractionated into 7 groups, methanol extract, hexane fraction(fr.), methanol soluble fr., dichloromethane fr., ethylacetate fr., butanol fr. and aqueous fr.. Chinese cabbage kimchi fractions inhibited the growth of AGS and HT 29 cancer cells as dose dependent. In particular, the dichloromethane fr. showed the highest inhibitory effect among other fractions. When the dichloromethane fr.(0.2mg/ml) was treated, the number of AGS and HT 29 survival cancer cells reduced to 12$\times$104/ml and 11$\times$104/ml compared to 166$\times$104/ml and 50$\times$104/ml of the controls, respectively. Chinese cabbage kimchi fractions also inhibited the DNA synthesis of the cancer cells. They inhibited the DNA synthesis of AGS human gastric adenocarcinoma cells more efficiently than that of HT 29 human colon adenocarcinoma cells. These results indicate that Chinese cabbage kimchi fractions show in vitro anticancer activity and the dichloromethane fr. among them reveals the highest effect.

• Food Science and Biotechnology
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• v.16 no.2
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• pp.260-264
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• 2007

Gleditsiae Semen (GS) has been used in both Korea and China as herbal medicine for the treatment of cephalalgia, catharsis, and other diseases. However, the apoptosis of GS against human cancer cells has not previously been investigated. The primary objective of this study was to determine the mechanisms inherent in GS-induced cytotoxicity and apoptosis, using methanolic extract of GS (GSE) in HT-29 human colon carcinoma cells. We found that GSE induced cytotoxicity in HT-29 cells in a dose-dependent manner, and this effect was verified via a lactate dehydrogenase release assay and a colony formation assay. In particular, HT-29 cells showed extensive cell death when treated with $50\;{\mu}g/mL$ of GSE; the calculated $IC_{50}$ value was $20\;{\mu}g/mL$. It induced characteristic apoptotic signs in HT-29 cells, including chromatin condensation and DNA fragmentation, occurring within 6-24 hr when the cells were treated at a concentration of $50\;{\mu}g/mL$. Interestingly, we detected the activation of caspase-3 and -9, but not caspase-8, and apoptotic bodies in GSE-treated HT-29 cells. Collectively, our results indicate that GSE induces apoptosis via a mitochondria-mediated apoptotic pathway, and these findings may be significant with regard to the development of a new drug for the treatment of human colon carcinoma cells.