• IMMUNE NETWORK
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• v.12 no.5
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• pp.189-195
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• 2012

It has been reported that vitamin C plays an effective role in the treatment and prevention of cancer, but its specific mechanisms are still largely unknown. The incidence of colon cancer is now increasing in Korea. Therefore, we have examined here the effect of vitamin C on the induction of the apoptosis on colon cancer and its related mechanisms. We have found that remarkable increase of the apoptosis and the calcium influx in endoplasmic reticulum (ER) in human colon cancer cell line, HCT-8. However, vitamin C-induced apoptosis was effectively inhibited by the pre-treatment of BAPTA-AM (1,2-bis(o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid), which is well-known as a calcium specific chelator. During the apoptosis, we found the increase of the translocation of Bad to mitochondria from cytosol, after releasing from 14-3-$3{\beta}$. In this process, the expression of Bax, a well-known pro-apoptotic protein, was also increased. Taken together, vitamin C induces apoptosis of colon cancer cell line, HCT-8 through the increase of 1) the calcium influx in endoplasmic reticulum (ER), 2) the translocation of Bad to mitochondria, and 3) the expression of Bax.

• BMB Reports
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• v.41 no.11
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• pp.803-807
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• 2008

We investigated the expression of muscarinic acetylcholine receptors (mAChRs) and their possible involvement in the regulation of cell proliferation in four colon cancer cell lines (SNU-61, SNU-81, SNU-407, and SNU-1033) derived from Korean colon carcinoma patients. A ligand binding assay showed that all four cell lines expressed mAChRs. Treatment of the four cell lines with the cholinergic agonist carbachol led to the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). In SNU-407 cells, carbachol significantly stimulated cell proliferation, which could be abolished by the muscarinic antagonist atropine and the ERK1/2 kinase inhibitor PD98059. These results indicate that mAChRs specifically mediate the proliferation of SNU-407 colon cancer cells via the ERK1/2 pathway.

• Journal of Nutrition and Health
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• v.37 no.1
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• pp.31-37
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• 2004

Curcumin, a natural compound extracted from rhizomes of Curcuma longa, has been shown to possess potent anti-inflammatory and anti-tumor activity. The mechanism by which curcumin initiates apoptosis remains poorly understood. In this study, we investigated the effects of curcumin on caspase-3 activity and protein expression of procaspase-3, Bcl-2, Bax, total Akt and phosphorylated Akt in SW480 human colon cancer cell. We cultured SW480 cells in the presence of various concentrations (0, 10, 20 or 30 uM) of curcumin. Curcumin inhibited colon cancer cell growth in a dose-dependent manner (p < 0.05). Caspase-3 activity was significantly increased dose-dependently in cells treated with curcumin (p < 0.05), concisely procaspase-3 expression was significantly decreased. Bcl-2 levels were decreased dose-dependently in cells treated with curcumin (p < 0.05), but Ben remained unchanged. In addition, phosphorylated Akt levels and total Akt levels were markedly lower in cells treated with 20 uM of curcumin treatment (p < 0.05), In conclusion, we have shown that curcumin inhibits cell growth and induces apoptosis in SW480 human colon cancer cell lines via Akt signal pathway.

• Archives of Pharmacal Research
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• v.19 no.4
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• pp.261-263
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• 1996

SK-302B, an antibiotic purified from soil Streptomyces sp. 302, was structurally identified as echinomycin (C/sub 50/H/sub 66/N/sub 11/S/sub 2/). In the present experiment, the possibility of SK-302B as an anticolon cancer agent was investigated by using chemosensitivity system (MTT assay, clonogenic assay). Treatment of SK-302B on various colon cancer cell lines resulted in a significant cytotoxicity and tumor colony formation inhibition. These studies showed that SK-302B had a potent inhibition on colon cancer cells.

• 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.

• Journal of Nutrition and Health
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• v.31 no.4
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• pp.799-808
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• 1998

To investigate the antitumor activity of mugwort (Artemisia princeps Pampan), petroleum ether extract of mugwork was partially purified by a silica gel chromatography. Among several fractions, the fraction which was obtained under the elution with acetone, showed potent cytotoxicity against mouse leukemia cell line(Ll210), human colon cancer cell line (HCT-48) and human hepatoma cell line (Hep G2) , but was less effective with normal cell line(mouse embryo cell). Acetone fraction appeared to be glycolipid by Benedict test and the major fatty acids of the lipid were C16 ; 0 , C 18: 3by GC/MS analysis.

• Biomolecules & Therapeutics
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• v.15 no.2
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• pp.95-101
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• 2007

Resveratrol (3,5,4’-trihydroxy-trans-stilbene), a naturally occurring phytoallexin abundant in grapes and several plants, has been shown to be active in inhibiting proliferation and inducing apoptosis in several human cancer cell lines. On the line of the biological activity of resveratrol, a variety of resveratrol analogs were synthesized and evaluated for their growth inhibitory effects against several human cancer cell lines. In the present study, we found that one of the resveratrol analogs, 3,4,5-trimethoxy-4’-bromo-cis-stilbene, markedly suppressed human colon cancer cell proliferation (EC$_{50}$ = 0.01 ${\mu}$g/ml), and the inhibitory activity was superior to its corresponding trans-isomer (EC$_{50}$ = 1.6 ${\mu}$g/ml) and resveratrol (EC$_{50}$ = 18.7 ${\mu}$g/ml). Prompted by the strong growth inhibitory activity in cultured human colon cancer cells (Col2), we investigated its mechanism of action. 3,4,5-Trimethoxy-4’-bromo-cis-stilbene induced arrest of cell cycle progression at G2/M phase and increased at sub-G1 phase DNA contents of the cell cycle in a time- and dose-dependent manner. Colony formation was also inhibited in a dose-dependent manner, indicating the inhibitory activity of the compound on cell proliferation. Moreover, the morphological changes and condensation of the cellular DNA by the treatment of the compound were well correlated with the induction of apoptosis. These data suggest the potential of 3,4,5-trimethoxy-4’-bromo-cis-stilbene might serve as a cancer chemotherapeutic or chemopreventive agent by virtue of arresting the cell cycle and inducing apoptosis for the human colon cancer cells.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6349-6355
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• 2012

Previous studies showed that Math1 homologous to human Hath1 can cause mouse goblet cells to differentiate. In this context it is important that the majority of colon cancers have few goblet cells. In the present study, the potential role of Hath1 in colon carcinogenesis was investigated. Sections of paraffin-embedded tissues were used to investigate the goblet cell population of normal colon mucosa, mucosa adjacent colon cancer and colon cancer samples from 48 patients. Hath1 and Muc2 expression in these samples were tested by immunohistochemistry, quantitative real-time reverse transcription -PCR and Western blotting. After the recombinant plasmid, pcDNA3.1(+)-Hath1 had been transfected into HT29 colon cancer cells, three clones were selected randomly to test the levels of Hath1 mRNA, Muc2 mRNA, Hath1, Muc2, cyclin D1 and p27 by quantitative real-time reverse transcription-PCR and Western blotting. Moreover, the proliferative ability of HT29 cells introduced with Hath1 was assessed by means of colony formation assay and xenografting. Expression of Hath1, Muc2, cyclin D1 and p27 in the xenograft tumors was also detected by Western blotting. No goblet cells were to be found in colon cancer and levels of Hath1 mRNA and Hath1, Muc2 mRNA and Muc2 were significantly down-regulated. Hath1 could decrease cyclin D1, increase p27 and Muc2 in HT29 cells and inhibit their proliferation. Hath1 may be an anti-oncogene in colon carcinogenesis.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8563-8566
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• 2016

Colorectal cancer is one of the most common lethal cancer types worldwide. In recent years, widespread and large-scale studies have been done on medicinal plants for anti-cancer effects, including Glycyrrhiza glabra. The aim of this study was to evaluate the effects of an ethanol extract Glycyrrhiza glabra on the expression of HSP90, growth and apoptosis in the HT-29 colon cancer cell line. HT-29 cells were treated with different concentrations of extract (50,100,150, and $200{\mu}g/ml$). For evaluation of cell proliferation and apoptosis, we used MTT assay and flow cytometry technique, respectively. RT-PCR was also carried out to evaluate the expression levels of HSP90 genes. Results showed that Glycyrrhiza glabra inhibited proliferation of the HT-29 cell line at a concentration of $200{\mu}g/ml$ and this was confirmed by the highest rate of cell death as measured by trypan blue and MTT assays. RT-PCR results showed down-regulation of HSP90 gene expression which implied an ability of Glycyrrhiza glabra to induce apoptosis in HT-29 cells and confirmed its anticancer property. Further studies are required to evaluate effects of the extract on other genes and also it is necessary to make an extensive in vivo biological evaluation and subsequently proceed with clinical evaluations.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.6
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• pp.2569-2574
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• 2015

Necroptosis, also known as "programmed necrosis", has emerged as a critical factor in a variety of pathological and physiological processes and is considered a cell type-specific tightly regulated process with mechanisms that may vary rather greatly due to the change of cell line. Here we used HT-29, a human colon cancer cell line, to establish a necroptosis model and elucidate associated mechanisms. We discovered that cobalt chloride, a reagent that could induce hypoxia-inducible $factor-1{\alpha}(HIF1{\alpha})$ expression and therefore mimic the hypoxic microenvironment of tumor tissue in some aspects induces necroptosis in HT-29 cells when caspase activity is compromised. On the other hand, apoptosis appears to be the predominant death form when caspases are functioning normally. HT-29 cells demonstrated significantly increased RIPK1, RIPK3 and MLKL expression in response to cobalt chloride plus z-VAD treatment, which was accompanied by drastically increased $IL1{\alpha}$ and IL6 expression, substantiating the notion that necrosis can induce profound immune reactions. The RIPK1 kinase inhibitor necrostatin-1 and the ROS scavenger NAC each could prevent necrosis in HT-29 cells and the efficiency was enhanced by combined treatment. Thus by building up a necroptosis model in human colon cancer cells, we uncovered that mechanically RIP kinases collaborate with ROS during necrosis promoted by cobalt chloride plus z-VAD, which leads to inflammation. Necroptosis may present a new target for therapeutic intervention in cancer cells that are resistant to apoptotic cell death.