• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.4
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• pp.633-640
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• 2004

This study was performed to investigate the cytotoxic effect of the water-extract from Chaga mushroom (Inonotus obliquus) compositions containing powdered green tea in HCT-15 human colon carcinoma, AGS human gastric carcinoma and NIH3T3 mouse normal fibroblast cells using viable cell count and MTT assay. The water-extract from Chaga mushroom compositions induced inhibitory effects on proliferation of HCT-15 and AGS cells in the MTT assay and viable cell count. However, mouse normal NIH3T3 cells were exhibited 80% survival under the same condition. Chaga mushroom compositions showed highly antiproliferative effect in human cancer cell line HCT-15 and AGS, but not in mouse normal cell line NIH3T3. These results suggest that Chaga mushroom (Inonotus obliquus) compositions containing powdered green tea are the candidate for chemoprevention in colon and gastric cancer.

• Journal of Life Science
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• v.17 no.5 s.85
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• pp.671-677
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• 2007

This study was performed to investigate the effect of the water-extract from non-fermented or fermented Chaga mushrooms (Inonotus obliquus) on the proliferation and apoptosis of the NIH3T3 mouse normal fibroblast cells and various human cancer cell lines including HCT-15 human colon carcinoma, AGS human gastric carcinoma, MCF-7 human breast adenocarcinoma, Hep3B human hepatocellular carcinoma and HeLa human cervical carcinoma using MTT(3-[4,5-dimethylthiazol-2-yl] -2,5-diphenyl tetrazolium bromide) assay and DNA fragmentation. In an anti-cancer test using various human cancer cells, fermented Chaga mushroom extract showed higher antiproliferating effect than that of non-fermented Chaga mushroom extract. Mouse normal NIH3T3 cells were exhibited 80% above survival under fermented or non-fermented Chngn mushroom extract of various concentrations(0, 0.5 and 1 mg/ml). Fermented Chaga mushroom extract significantly inhibited cell growth on HCT-15 cells in a dose-dependent manner. HCT-15 cells treated with non-fermented or fermented Chaga mushrooms extract produced a distinct oligonucleosomal ladder with different sizes of DNA fragments, a typical characteristic of cells undergoing apoptosis. These results suggest that fermented Chaga mushroom extract suppresses growth of HCT-15 human colon carcinoma cells through apoptosis.

• Applied Biological Chemistry
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• v.47 no.2
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• pp.202-207
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• 2004

This study was performed to investigate the inhibitory effect of the water-extract from fermented compositions containing Inonotus obliquus with added Houttuynia cordata on the growth of either human AGS gastric and HCT-15 colon cancer cells or NIH3T3 normal mouse fibroblast cells. Cytotoxic activity on cancer cells was investigated by viable cell count, MTT assay and morphological observation. Mixtures of Inonotus obliquus with added Houttuynia cordata were fermented at $30{\sim}37^{\circ}C$, $50{\sim}60%$ humidity for 30 days, extracted with water, freeze dried, powered, and then dissolved in water for the experiment. In MTT assay, the fermented compositions exhibited inhibitory effects of 13, 25, 40, 67 and 78% for AGS and 22, 40, 50, 69 and 76% for HCT-15 at 0.16, 0.4, 0.8, 1.6 and 4.0 mg/ml, respectively. However, normal NIH3T3 cells were exhibited 86% survival under the same experimental condition. Fermented compositions showed highly inhibitory effect against human cancer cell line HCT-15 and AGS, but not on normal cell line NIH3T3.

• Animal cells and systems
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• v.1 no.3
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• pp.521-526
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• 1997

We isolated a mouse nck cDNA from the thymus cDNA expression library. The cDNA encodes a 377 amino acid protein and displays 97% amino acid sequence identity to human oncogenic protein nck, which is composed almost exclusivelv of three src homology 3 (SH3) domains and one SH2 domain. The sequence analysis also showed that the isolated cDNA is the mouse counterpart of the human nck and different from the mouse grb4, which has been reported to be highly similar to the human nck and, therefore considered as a mouse nck, Northern blot analysis showed that the transcript of the gene was 1.8 kb and was highly expressed in the testis, thymus, and brain but moderately in the liver and lymph node. Western blot analysis showed that the size of the protein was about 47 kDa. Overexpression of the mouse Nck transformed a mouse fibroblast cell line, NIH3T3. The results clearly indicate that normal nck gene has transforming ability and provide an argument against a suggested possibility that the transforming ability of the human nck gene is due to a mutation(s) in the gene.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.6
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• pp.1314-1319
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• 2009

In previous study, we have shown that continentalic acid (CA) isolated from Aralia continentalis induced the growth inhibition and apoptosis in HepG2 cells. In this study, we examine the effects of CA from A. continentalis on growth inhibition and apoptosis induction in human leukemia HL-60 and mouse fibroblast NIH 3T3 cell lines. The results demonstrated that CA decreased cell growth of leukemia HL-60 cells but not human HaCaT keratinocytes, assessed with the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] and LDH (lactate dehydrogenase) assay. Flow cytometric analysis of mouse fibroblast cell lines exposed to CA showed that apoptotic cells increased in a time- and dose-dependent manner. Treatment with CA decreased the number of normal cells and increased the number of early apoptotic and late apoptotic cells in a dose-dependent manner. The induction of apoptosis in mouse cell lines by CA was mediated through the activation of caspase-3, Bak, and Bax and the down-regulation of Bcl-2. Our results suggest that CA efficiently induces apoptosis in human leukemia cells.

• BMB Reports
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• v.49 no.2
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• pp.99-104
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• 2016

The nuclear non-histone protein high mobility group box (HMGB) 1 is known to having an inhibitory effect on the repair of DNA damaged by the antitumor drug cisplatin in vitro. To investigate the role of HMGB1 in living cells, we studied the DNA repair of cisplatin damages in mouse fibroblast cell line, NIH-3T3. We evaluated the effect of the post-synthetic acetylation and C-terminal domain of the protein by overexpression of the parental and mutant GFP fused forms of HMGB1. The results revealed that HMGB1 had also an inhibitory effect on the repair of cisplatin damaged DNA in vivo. The silencing of HMGB1 in NIH-3T3 cells increased the cellular DNA repair potential. The increased levels of repair synthesis could be "rescued" and returned to less than normal levels if the knockdown cells were transfected with plasmids encoding HMGB1 and HMGB1 K2A. In this case, the truncated form of HMGB1 also exhibited a slight inhibitory effect.

• Journal of Life Science
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• v.21 no.6
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• pp.767-774
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• 2011

Cell migration plays a fundamental role in cancer cell invasion and metastasis as well as in many physiological responses. Here, we screened four different sources of garlic - water extract of normal and black garlic, as well as dried normal and black garlic - for the identification of anti-invasive and anti-metastatic activity on cancer cells. Inhibition of cancer cell migration was observed in the hexane extract of dried-garlic. Inhibitory activity was further purified to near homogeneity by thin layer chromatography and named $\b{i}$nhibitor of $\b{c}$ancer $\b{m}$etastasis from garlic #27 (ICMG-27). ICMG-27 completely blocked insulin-like growth factor-1 (IGF-1)-induced OVCAR-3 cell migration at 6 ${\mu}g/ml$. ICMG-27 completely blocked IGF-1-induced OVCAR-3 and NIH-3T3 cell migration whereas IGF-1-induced mouse embryonic fibroblast (MEF) cell migration was not affected byICMG-27. ICMG-27 inhibited all the tested IGF-1-induced cancer cell migration such as OVCAR-3, SKOV-3, and MDA-MB-231 cells. Finally, ICMG-27 could inhibit IGF-1-, lysophosphatidic acid (LPA)-, sphingosine-1-phosphate (S1P)-, leukotriene B4 (LTB4)-, and angiotensin II (AngII)-induced OVCAR-3 cell migration. These results indicate that ICMG-27 inhibits cancer cell migration by blocking essential steps in many agonists-induced cancer cell migrations. Unveiling an anti-invasive mechanism of ICMG-27 on cancer cells will provide a basis for cancer therapy.