• Journal of Life Science
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• v.17 no.9 s.89
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• pp.1232-1236
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• 2007

Growth and DNA synthesis inhibitory effects of extracts from root bark of Ulmus parvifolia on MG-63 human osteosarcoma cells, HT-29 human colon cancer cells and K-562 leukemia cancer cells were studied. The root bark extract of Ulmus parvifolia was extracted with methanol, hot water and juice. The methanol extract showed the highest inhibitory effect on growth of MG-63, HT-29 and K-562 cancer cells by >85%. The treatment of hot water and juice extracts from root bark of Ulmus parvifolia also inhibited growth of the above cancer cells with increasing concentration. DNA synthesis of MG-63 and HT-29 cancer cells was significantly inhibited by adding methanol, hot water and juice extracts from root bark of Ulmus parvifolia with increasing concentration, showing that the inhibitory effect of growth was more effective on HT-29 cancer cells. These results suggest that the methanol extract from root bark of Ulmus parvifolia may have specific active com-pounds on anticancer effect. The hot water extract also showed a strong inhibitory effect on growth of cancer cells, indicating that the active compounds may be stable to heat.

• 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)

• Korean Journal of Pharmacognosy
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• v.37 no.3
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• pp.130-135
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• 2006

The present study describes the preliminary evaluation of the cytotoxic activity of the extracts from Inula japonica. I. japonica was extracted with methanol, ethanol, acetone, and water, and then cytotoxic activity of these extracts were evaluated. The cytotoxic activity of each extract was assessed by the MTT-dye reduction assay. Both ethanol and acetone extracts from I. japonica showed the cytotoxic activity against the HT-29 human colon cancer cells. Furthermore, the ethanol extract was fractionated with n-hexane, diethyl ether, ethyl acetate, and water according to degree of Polarity, The diethyl ether fraction showed the highest cytotoxic activity against HT-29 cells, but the other fractions showed low cytotokic activity. In addition, diethyl ether layer also showed the cytotoxic activity against various tumor cells, such as human colon carcinoma SW620, human cervix adenocarcinoma HeLa, and human breast adenocarcinoma MCF-7 cells as well as HT-29 cells. These studies support that extracts of I. japonica may be a potential candidate as possible chemotherapeutic agent against human cancer.

• 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.27 no.5
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• pp.545-552
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• 2017

Julbernardia globiflora, a tropical African tree widespread in Miombo woodland, has been used in folk medicine for the treatment of depression and stomach problems. However, the antioxidative and anticancer activities of J. globiflora remain unclear. The objective of this study is to evaluate the antioxidative and anticancer effects of methanol extract of J. globiflora (MEJG) and the molecular mechanism of its anticancer activity in human colon carcinoma HT29 cells. MEJG exhibited significant antioxidative effect with an $IC_{50}$ (concentration at 50% inhibition) value of $1.23{\mu}g/ml$ measuring by 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay and inhibited cell proliferation in a dose-dependent manner in HT29 cells. We found that MEJG induced apoptosis of HT29 cells with the increase of apoptotic cells and apoptotic bodies using Annexin V staining and 4,6-diamidino-2-phenylindole (DAPI) staining, respectively. The MEJG treatment showed the increase of Fas, a death receptor, and Bax, a pro-apoptotic protein, and the decrease of Bcl-2, an anti-apoptotic protein, resulting in the release of cytochrome c from the mitochondria into the cytosol and activation of caspase-3, -8 and -9. The apoptotic effects of MEJG were confirmed by cleavage of poly (ADP-ribose) polymerase (PARP). Collectively, these results suggest that MEJG may exert the anticancer effect in HT29 cells by inducing apoptosis via both the intrinsic and extrinsic pathways.

• Preventive Nutrition and Food Science
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• v.7 no.3
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• pp.250-254
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• 2002

The anticancer effects of leek (buchu in Korean) kimchi were evaluated in the human cancer cells: AGS gastric adenocarcinoma cells, HT-29 human colon adenocarcinoma cells and HL-60 leukemia cells. The leek kimchi (fermented for 6 days at 15$^{\circ}C$) was fractionated into 7 groups: methanol extract, hexane extract, methanol soluble extract MSE), dichloromethane (DCM) fraction (fr.), ethyl acetate fr., butanol fr. and aqueous fr. Most of the leek kimchi tractions inhibited the growth of AGS and HT-29 cancer cells in a dose dependent manner. In particular, the DCM fr. showed the highest inhibitory effect among the tractions. Treatment with the DCM fr. (0.1 mg/mL) reduced the survival rates of AGS and HT-29 cancer cells to 19% and 37% of the controls, respectively. Moreover the DCM fr. of the leek kimchi arrested G2/M phase in the cell cycle and induced apoptosis in HL-60 human promyelocytic leukemia cells. These results indicate that the leek kimchi exerted an anticancer effect on those human cancer cells, and that the DCM fr. arrested G2/M phase in the cell cycle and induced apoptosis in the leukemia cells.

• Archives of Pharmacal Research
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• v.29 no.3
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• pp.209-212
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• 2006

We investigated the effect of protein extract of Asterina pectinifera on the activity of 4 enzymes that may playa role in adenocarcinoma of the colon: quinone reductase (QR), glutathione Stransferase (GST), ornithine decarboxylase (ODC), and cyclooxygenase (COX)-2. QR and GST activity increased in HT-29 human colon adenocarcinoma cells increased that had been exposed to 4 concentrations of the protein extract (80, 160, 200, and $240{\mu}g/mL$). Additionally, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ODC activity decreased significantly in cells exposed to the extract in concentrations of $160{\mu}g/mL$ (p<0.05), $200{\mu}g/mL$ (p<0.005), and $240{\mu}g/mL$ (p<0.005). TPA-induced COX-2 activity also decreased in cells exposed to extract concentrations of 10, 20, 40, and $60{\mu}g/mL$. COX-2 expression was also inhibited in cells exposed to this extract. These results suggest that this protein extract of A pectinifera has chemopreventive activity in HT-29 human colon adenocarcinoma cells, and therefore, may have the potential to function as a chemopreventive agent in human colorectal cancer.

• 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.

• Food Engineering Progress
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• v.15 no.1
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• pp.64-69
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• 2011

The anticancer activity of Schizandra chinensis Baillon was investigated for the development of functional food resources. The antiproliferative activity of hot water extracts of Schizandra chinensis Baillon in human colon cancer cell line (HT-29) were identified using cell viability, morphology study, cell cycle and RT-PCR analyses. HT-29 cells were cultured in several concentrations (0, 1.0, 2.0, 4.0 mg/mL) of water extracts of Schizandra chinensis Baillon. In our study, colon cancer cell growth could be inhibited by hot water extracts of Schizandra chinensis Baillon in a dose-dependent manners. It was associated with morphological changes and apoptotic cell death with cell shrinking, chromatin condensation, apoptotic bodies and cell cycle analysis. These results suggest that Schizandra chinensis Baillon may inhibit the growth of human colon cancer cells by various apoptosis-aiding activities as well as apoptosis itself.

• Journal of Acupuncture Research
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• v.31 no.2
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• pp.87-98
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• 2014

Objectives : We investigated whether snake venom toxin(SVT) from Vipera lebetina turanica sensitizes HT29 human epithelial colorectal cancer cells to tumor necrosis factor(TNF)-related apoptosis-inducing ligand(TRAIL) induced apoptosis in cancer cells. Methods : Cell viability assay was used to assess the inhibitory effect of TRAIL on cell growth of HT29 human colorectal cancer cells. And 6-diamidino-2-phenylindole(DAPI), terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay(TUNEL) staining assay were used to evaluate cell-apoptosis. Western blot analysis were conducted to observe apoptosis related proteins and death receptor. To assess whether the synergized inhibitory effect of SVT and TRAIL on reactive oxygen species(ROS) generation was reversed by strong anti-oxidative agent. Results : SVT with TRAIL inhibited HT29 cell growth different from TRAIL alone. Consistent with cell growth inhibition, the expression of TRAIL receptors; Expression of death receptor(DR)4 and DR5 was significantly increased and intrinsic pro-apoptotic cleaved caspase-3, -9 was subsequently increased together with increase of Bax/Bcl-2 ratio and extrinsic pro-apototic caspase-8 was also activated. In addition, the expression of anti-apoptotic survival proteins, a marker of TRAIL resistance(eg, cFLIP, survivin, X-linked inhibitor of apoptosis protein(XIAP) and Bcl-2) was suppressed by the combination treatment of SVT and TRAIL. Pretreatment with the ROS scavenger N-acetylcysteine abolished the SVT and TRAIL-induced upregulation of DR4 and DR5 expression and expression of the intrinsic pro-apoptotic caspase-3 and-9. Conclusion : The collective results suggest that SVT facilitates TRAIL-induced apoptosis in $HT_{29}$ human epithelial colorectal cancer cells through up-regulation of the TRAIL receptors; DR4 and DR5 and consecutive induction of bilateral apoptosis via regulating apoptosis related proteins.