• 한국식품영양학회지
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• 제22권2호
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• pp.308-312
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• 2009

저분자량 키토산 올리고당의 세포 독성을 실험하였다. 저분자량 키토산 올리고당은 정상세포주인 Vero E6(Africa green monkey kidney cell)에 대한 세포 독성을 거의 나타내지 않았다. 정상세포주에 대한 저분자량 키토산 올리고당의 $IC_{50}$값은 $1,060.28{\mu}g/m{\ell}$이었다. 저분자량 키토산 올리고당은 폐암 세포주인 A549, 방광암 세포주인 J82, 대장암 세포주인 SNU-C4, 위암 세포주인 SNU-1, 유방암 세포주인 ZR75-1 등과 같은 사람의 종양세포주에 대한 in vitro 항종양성을 나타내었다. 종양세포주에 대한 저분자량 키토산 올리고당의 $IC_{50}$값은 A549, J82, SNU-C4, SNU-1, ZR75-1 세포주의 경우에 각각 $477.42{\mu}/m{\ell}$, $480.40{\mu}g/m{\ell}$, $436.84{\mu}g/m{\ell}$, $373.55{\mu}g/m{\ell}$, and $539.95{\mu}/m{\ell}$이었다.

• 대한핵의학회지
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• 제34권4호
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• pp.294-302
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• 2000

목적: 종양세포에서 F-18-FDG 섭취 기전을 규명하기 위하여 F-18-FDG 섭취와 포도당운반체-1 (Glut-1), hexokinase의 발현과의 상관관계를 조사하였다. 대상 및 방법: 사람의 대장암(SNU-C2A, SNU-C4, SNU-C5), 간암(SNU-387, SNU-423, SNU-449), 폐암(NCI-H522, NCI-H358, NCI-H1299), 자궁경부암(HeLa, HeLa 229, HeLa S3), 그리고 뇌암(A172, Hs 683)에서 기원한 암 세포주 $5{\times}10^5$ 세포를 24 well plate에 24시간 배양하였다. 여기에 37 kBq의 F-18-FDG를 첨가한 후 각 세포의 섭취 정도를 감마 카운터를 사용하여 측정하였다. Hexokinase의 활성은 분광광도계를 사용하여 측정하였다. 디토콘드리아에서의 hexokinase 활성은 고속원심분리기를 이용하여 미토콘드리아 분획을 분리하여 조사하였다. Glut-1의 발현은 면역조직염색법으로 측정하였다. 결과: 종양세포의 종류에 따라 F-18-FDG 섭취, 전체 그리고 미토콘드리아 hexokinase 활성, 그리고 Glut-1의 발현 정도에 차이가 있었다. 종양세포주에서 F-18-FDG 섭취와 세포전체, 세포내 미토콘드리아 hexokinase 활성과의 상관관계(각각 r=0.27, r=0.26)는 낮게 나타났으며, Glut-1의 발현은 F-18-FDG의 섭취와 상관관계(p=0.81, p=0.0015)가 높았다. 대장암 세포주에서 F-18-FDG 섭취와 hexokinase 활성의 상관관계가 없다는 보고를 토대로 대장암 세포주 결과를 제외했을 경우에 F-18-FDG의 섭취와 세포전체 그리고 세포내 미토콘드리아에서의 hexokinase 활성과는 높은 상관관계(각각 r=0.81, p=0.0027, 그리고 r=0.81, p=0.0049)를 보였다. 결론: Glut-1이나 hexokinase 활성이 사람 종양 세포주에서 F-18-FDG의 섭취를 결정하는 주 요인이며, 종양세포의 종류에 따라 이들의 기여도는 서로 다름을 알 수 있었다.

• 대한약침학회지
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• 제15권3호
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• pp.19-30
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• 2012

Objectives: Many efforts have shown multi-oncologic roles of galectin-3 for cell proliferation, angiogenesis, and apoptosis. However, the mechanisms by which galectin-3 is involved in cell proliferation are not yet fully understood, especially in human colon cancer cells. Methods: To cluster genes showing positively or negatively correlated expression with galectin-3, we employed human colon cancer cell lines, SNU-61, SNU-81, SNU-769B, SNU-C4 and SNU-C5 in high-throughput gene expression profiling. Gene and protein expression levels were determined by using real-time quantitative polymerase chain reaction (PCR) and western blot analysis, respectively. The proliferation rate of human colon cancer cells was measured by using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Results: Expression of ${\gamma}$-aminobutyric acid B receptor 1 (GABABR1) showed a positive correlation with galectin-3 at both the transcriptional and the translational levels. Down-regulation of galectin-3 decreased not only GABABR1 expression but also the proliferation rate of human colon cancer cells. However, Korean herbal extract, HangAmDan-B (HAD-B), decreased expression of GABABR1 without any expressional change of galectin-3, and offset ${\gamma}$-aminobutyric acid (GABA)-enhanced human colon cancer cell proliferation. Conclusions: Our present study confirmed that GABABR1 expression was regulated by galectin-3. HAD-B induced galectin-3-independent down-regulation of GABABR1, which resulted in a decreased proliferation of human colon cancer cells. The therapeutic effect of HAD-B for the treatment of human colon cancer needs to be further validated.

• BMB Reports
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• 제33권2호
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• pp.184-187
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• 2000

Prostaglandin $E_2$ ($PGE_2$) plays an important role in the regulation of various gastric functions, and the growth-inhibitory activities on tumor cells are studied in vitro and in vivo. Although the mechanisms have attracted many researchers in the past decade, the molecular mechanisms of cell cycle arrest, or induction of apoptosis by $PGE_2$, is unclear. We investigated the effects of $PGE_2$ on the growth of the human gastric carcinoma cell line SNU1 and genes that are regulated by $PGE_2$ and isolated them using differential display RT-PCR (DD RT-PCR). FACS analysis suggested that SNU1 cells were arrested at the G1 phase by $PGE_2$ treatment. This growth inhibitory effect was in a time- and dose-dependent manner. Treatment of SNU1 cells with $10\;{\mu}g/ml$ $PGE_2$, followed by DD RT-PCR analysis, revealed differently expressed bands patterns from the control. Among the differently expressed clones, we found an unidentified cDNA clone (HGP-27) overexpressed in $PGE_2$-treated cells. The full-length cDNA of HGP-27 was isolated using RACE, which consisted of a 30-nt 5'-noncoding region, a 891-nt ORF encoding the 296 amino acid protein, and a 738-nt 3'-noncoding region including a poly(a) signal. This gene was localized on the short arm of chromosome number 11. Using the Motif Finder program, a myb-DNA binding repeat signature was detected on the ORF region. The COOH-terminal half was shown to have similarity with the $NH_3$-terminal domain of thioredoxin (Trx). This relation between HGP-27 and Trx implied a potential role for HGP-27 in modulating the DNA binding function of a transcription factor, myb.

• 대한본초학회지
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• 제21권1호
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• pp.33-42
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• 2006

Objectives : The purpose of this study was to investigate the anticancer effects of Bodusan (BDS) on SNU-1 cells, a human gastric cancer cell line. Methods : To study the cytotoxic effect of BDS on SNU-1 cells, the cells were treated with various concentrations of BDS and then cell viability was determined by XTT reduction method and trypan blue exclusion assay. The typical signs of apoptosis, was examined by western blot analysis. BDS-induced MAPK activation was also examined by Western blot for phosphorylated ERK and p38. Results : BDS reduced proliferation of SNU-1 cells in a dose-dependent manner and decreased procaspase 3 level in a dose-dependent manner and induced the clevage of PARP at concentration > 500 ${\mu}g/ml$. BDS also triggered the mitochondrial apoptotic signaling by increasing the release of cytochrome C from mitochondria to cytosol and reducing the level of anti-apoptotic Bcl-2. BDS significantly decreased ERK phosphorylation and increased p38 phosphorylation in a dose-dependent manner. Futhermore, BDS treatment up-regulated p53 and p21waf expression in a dose-dependent manner. Conclusion : BDS-induced apoptosis is MAP kinase-dependent apoptoric pathway and arrested SNU-1 cells at the G0/G1 of cell cycle. These results suggest that BDS is potentially useful as a chemotherapeutic agent in human gastric cancer.

• Journal of Electrochemical Science and Technology
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• 제2권4호
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• pp.204-210
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• 2011

Thin film electrodes have been intensively studied for active materials and current collectors to enhance the electrochemical performance. Here, porous structures of nickel-based oxide films, consisting of nickel oxide and copper (II) oxide, which was derived from the copper substrate during the annealing process, were deposited on metallic copper foils. The half-cell tests revealed excellent capacity retention after $80^{th}$ charge/discharge cycles. Some films showed an excess of the theoretical capacity of nickel oxides, which mainly originate from partially oxidized copper substrates during annealing. These results exhibit that both a preparation method of an active materials and partially oxidized current collectors could be important roles to apply thin film electrodes.

• 약학회지
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• 제38권3호
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• pp.311-321
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• 1994

Anticancer effects of Aloe on sarcoma 180 in ICR mouse or human cancer cells were determined. Sarcoma 180 cells were inoculated subcutaneously into male ICR mouse to determine effect of Aloe on tumor gowth, or inoculated intraperitoneally into male ICR mouse to determine effect of Aloe on life span prolongation, followed by oral administration of Aloe vera(10 mg/kg/day, 50 mg/kg/day) or Aloe arborescens(10 mg/kg/day, 100 mg/kg/day) once a day for 14 days. The administration of Aloe vera or Aloe arborescens did not suppress tumor growh. However the life span of ICR mouse was prolonged to 19%(p<0.05), 22%(p<0.05) and 32%(p<0.05) by administration of Aloe vera 10 mg/kg/day, Aloe vera 50 mg/kg/day, and Aloe arborescens 100 mg/kg/day, respectively. To determine anticancer effect of Aloe in vitro, Aloe extract was added to the culture of human gastric cancer cells(SNU-1) and colorectal cancer cells(SNU-C2A), and concentration of Aloe to inhibit cancer cell growth was determined using MTT(3-[ 4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) cytotoxicity assay. High $ID_{50}$ values of Aloe vera and Aloe arborescens against gastric cancer cell line(SNU-1) and colorectal cancer cell line(SNU-C2A) suggest that Aloe gel does not have anticancer effect on these specific human cancer cells although high concentration of Aloe inhibited growth of human cancer cells significantly.

• Biomolecules & Therapeutics
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• 제30권2호
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• pp.137-144
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• 2022

Radiation resistance represents an imperative obstacle in the treatment of patients with colorectal cancer, which remains difficult to overcome. Here, we explored the anti-proliferative and migration-inhibiting properties of the natural product shikonin on a radiation-resistant human colon carcinoma cell line (SNU-C5RR). Shikonin reduced the viability of these cells in a dose-dependent manner; 38 µM of shikonin was determined as the half-maximal inhibitory concentration. Shikonin induced apoptotic cell death, as demonstrated by increased apoptotic body formation and the number of TUNEL-positive cells. Moreover, shikonin enhanced mitochondrial membrane depolarization and Bax expression and also decreased Bcl-2 expression with translocation of cytochrome c from mitochondria into the cytosol. In addition, shikonin activated mitogen-activated protein kinases, and their specific inhibitors reduced the cytotoxic effects of shikonin. Additionally, shikonin decreased the migration of SNU-C5RR cells via the upregulation of E-cadherin and downregulation of N-cadherin. Taken together, these results suggest that shikonin induces mitochondria-mediated apoptosis and attenuates epithelial-mesenchymal transition in SNU-C5RR cells.

• Journal of Nutrition and Health
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• 제36권1호
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• pp.18-23
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• 2003

We studied the effects of hot water extract of Inonotus obliquos mushroom on the proliferation and apoptosis of the human colon adenocarcinoma, HT-29 and the human stomach adenocarcinoma, SNU-484 cell. Cells were maintained with Dulbecco's modified Eagle medium/Ham's F-12 nutrient mixture supplemented with 10% fetal bovine serum at 37$^{\circ}C$ in a humidified $CO_2$. For the cell proliferation experiments, cells were seeded in 35 mm dishes, and were treated with the various concentrations of the extract for the different time course. Apoptosis was measured by caspase-3 activity. When we incubated HT-29 cells for 24, 48, 72, and 96 hours after treatments, the cell proliferation was more suppressed with more treatment time. In case of the human stomach cancer cell, SNU484, the extract significantly decreased the cell number. Thus, the treatment of 1.5 mg/$m\ell$ extract decreased almost half of the cell number. Caspase-3 activity in HT-29 was increased by the treatment of mushroom extracts. In SNU484, caspase-3 activity tended to increase in proportion to the amounts of the extracts and the treatment of Inonotus obliquos affected the activity a lot. Therefore, Inonotus obliquos is suggested for the prevention of gastro-intestinal cancer and strongly recommended for the treatment of stomach cancer. (Korean J Nutrition 36(1) : 18~23, 2003)

• Archives of Pharmacal Research
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• 제21권5호
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• pp.599-609
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• 1998

In search for new antitumor agents, twelve 6-aziridinylbenzimidazole derivatives were synthesized and their cytotoxicities were tested against three cancer cell lines (mouse lymphocytic leukemia P388 and B16, and human gastric carcinoma SNU-16). From 4-amino-3-nitrotoluene as the starting material, 2-(acetoxymethyl)benzimidazoles (5a-d) were obtained by Phillips reaction. These benzimidazoles were then reacted with Fremy's salt to give a mixture of three 2-(acetoxymethyl) (8a-c) and four 2-(hydroxymethyl)benzimidazole-4,7-diones (9a-d). Addition of these quinones with aziridine afforded 6-aziridinyl-2-(acetoxymethyl) (10a-c) and 6-aziridinyl-2-(hydroxymethyl)benzimidazole-4,7-diones (11a-d). Utilizing 2-(hydroxymethyl)benzimidazole-4,7-diones (9b,d), esters 10d and 13e-h were prepared by the sequential reactions of esterification and addition. The synthesized compounds show potent cytotoxicity against all of three cell lines tested. The cytotoxicities of 10a-d or 11a-d against SNU-16 were wuperior to those of 13e-h, and were equal to or slightly higher than that of mitomycin C. compounds 11a-d were slightly more cytotoxic than 10a-d in all cell lines tested.