• BMB Reports
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• 제48권10호
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• pp.565-570
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• 2015

In several reports, the respiratory syncytial virus (RSV) was identified as an oncolytic virus in cancer cells (e.g., lung and prostate cancer). However, the effects of RSV in hepatocellular carcinoma (HCC) cells have not yet been investigated. Here, we observed the inhibitory effects of RSV infection in HCC cell-lines. Cell growth was significantly decreased by RSV infection in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. After RSV infection, plaque formation and syncytial formation were observed in affected Hep3B and Huh-7 cells. RSV protein-expression was also detected in Hep3B and Huh-7 cells; however, only Huh-7 cells showed apoptosis after RSV infection. Furthermore, inhibition of cell migration by RSV infection was observed in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. Therefore, further investigation is required to clarify the molecular mechanism of RSV-mediated inhibition of HCC cell growth, and to develop potential RSV oncolytic viro-therapeutics.

• 한국자원식물학회지
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• 제30권3호
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• pp.265-271
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• 2017

In this study, we elucidated the molecular mechanism of silymarin by which silymarin may inhibits cell proliferation in human colorectal cancer cells in order to search the new potential anti-cancer target associated with the cell growth arrest. Silymarin reduced the level of c-Myc protein but not mRNA level indicating that silymarin-mediated downregulation of c-Myc may result from the proteasomal degradation. In the confirmation of silymarin-mediated c-Myc degradation, MG132 as a proteasome inhibitor attenuated c-Myc degradation by silymarin. In addition, silymarin phosphorylated the threonine-58 (Thr58) of c-Myc and the point mutation of Thr58 to alanine blocked its degradation by silymarin, which indicates that Thr58 phosphorylation may be an important modification for silymarin-mediated c-Myc degradation. We observed that the inhibition of ERK1/2, p38 and $GSK3{\beta}$ blocked the Thr58 phosphorylation and subsequent c-Myc degradation by silymarin. Finally, the point mutation of Thr58 to alanine attenuated silymarin-mediated inhibition of the cell growth. The results suggest that silymarin induces the cell growth arrest through c-Myc proteasomal degradation via ERK1/2, p38 and $GSK3{\beta}-dependent$ Thr58 phosphorylation.

• 한국진공학회:학술대회논문집
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• 한국진공학회 2013년도 제45회 하계 정기학술대회 초록집
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• pp.93-93
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• 2013

To make the rationale design of interface between cell and artificial surface, many studies have been controlled influencing cue which can typically be divided into two central categories: chemical cues based on modification surface chemical properties containing attractive/repulsive molecules, and physical cues that may include applied tension/stress, electrical polarization, magnetic field, and topography. Recently, researches have been focused on physical cue, especially topography. The surface topography may influence cellular responses for example, cell adhesion, cell morphology and gene expression. However, there were few systematic studies about these nanotopographical effects on neuronal developments in a feature size-dependent manner. Herein, we report a nanoscale-resolved study of nanotopographical effects on cellular adhesion and growth. In this study, we use substrates with packed glass beads by rubbing method for generating highly periodic nanotopographies with various sizes. We found that acceleration of neuritogenesis appeared only on the beads larger than 200 nm in diameter, and observed that filopodial thickness was comparable with this scale. This study is expected to be essential to elucidate the nanotopographical effect on cellular adhesion and growth.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제30권1호
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• pp.30-40
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• 2008

The objectives of this study was to check up the effect of celecoxib, COX-2 inhibitor, on the pathogenesis of oral squamous cell carcinoma. After mefenamic acid, aspirin and celecoxib, COX-2 inhibitor, were inoculated to HN 22 cell line, the following results were obtained through tumor cell viability by wortmannin, growth curve of tumor cell line, apoptotic index, PGE2 synthesis, total RNA extraction, RT-PCR analysis and TEM features. 1. When wortmannin and celecoxib were given together, the survival rate of tumor cells was lowest about 47 %. So wortmannin had an effect on the decrease of survival rate of tumor cells. 2. In growth curve, the slowest growth was observed in celecoxib inoculated group. 3. The synthesis of PGE2 was decreased in all group and the obvious suppression and highest apoptotic index was observed in celecoxib inoculated group. 4. Suppression of expression of COX-2 mRNA was evident in celecoxib inoculated group. But that of COX-1,2 mRNA was observed in mefenamic acid inoculated group and aspirin inoculated group. 5. In celecoxib inoculated group, mRNA expression of AKT1 was decreased and that of PTEN & expression of caspase 3 and 9 was evidently increased. Depending on above results, when celecoxib was inoculated to oral squamous cell carcinoma cell line, an increase of mRNA expression of caspase 3,9 and PTEN is related to a decrease of mRNA expression of AKT1. Wortmannin had an effect on the decrease of survival rate of tumor cells. Celecoxib might induce apoptosis of tumor cell by suppression of AKT1 pathway and COX-2 inhibition. This results suggested that COX-2 inhibitor might be significantly effective in chemoprevention of oral squamous cell carcinoma.

• Journal of Acupuncture Research
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• 제22권6호
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• pp.37-50
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• 2005

Objectives : The purpose of this study was to investigate the anti-caner effect of Bee Venom and Melittin on the prostatic cancer cell(PC-3). The goal of study is to ascertain whether Bee Venom and Melittin inhibits the cell growth and cell cycle of PC-3, or the expression of relative genes and whether the regression of PC-3 cell growth is due to cell death or the expression of gene related to apoptosis. Methods : After the treatment of Pc-3 cells with Bee Venom and Melittin, we performed Fluorescence microscope, MTT assay, Western blotting, Flow cytometry, PAGE electrophoresis and Surface plasmon resonance analysis to identify the cell viability, apoptosis and gene related to apoptosis. Results : 1. Compared with Control cell, the inhibition of cell growth reduced in proportion with the dose of Bee Venom or Melittin($0{\sim}10{\mu}g/ml$) in PC-3. 2. In PC-3, Cell viabilities of Bee Venom or Melittin treatment was decreased significantly. 3. The nucli of Control cells were stained round and homogenous in DAPI staining, but those of PC-3 were stained condense and splitted. 4. In PC-3, apoptosis of Bee Venom or Melittin treatment was increased significantly. 5. Bax, Caspase-3 and P ARP of Bee Venom or Melittin treatment was increased significantly and Bcl-2 of Bee Venom or Melittin treatment was decreased significantly. Caspase-9 of Bee venom treatment was increased significantly. Conclusion : These results indicate that Bee Venom and Melittin inhibits the growth of prostate cancer cells, has anti-cancer effects by inducing apoptosis. We wish that the anti-cancer effects of Bee Venom and Melittin are used to clinical caner treatment.

• Biotechnology and Bioprocess Engineering:BBE
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• 제6권5호
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• pp.332-336
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• 2001

When parental Chinese hamster ovary (CHO) cell clones that are capable of producing thrombopoietin (TPO) were subjected to high methotrexate (MTX) concentrations, clonal variations in cell growth were apparent. In the clones that had no significant enhancement in specific TPO productivity (q$\_$Tpo/)when a higher level of MTX was administered, their growth was not depressed significantly nor their cell size changed significantly. On the other hand, those clones that showed a significant-enhancement in q$\_$Tpo/ at higher a MTX dosage, cell growth was depressed initially but recovered during successive sub-cultures. Furthermore, their cell size increased, which suggested that changes in cell size may be indicative of an enhanced q$\_$Tpo/. When the enhancement of the q$\_$Tpo/ of 9 clones after a high MTX dosage was plotted against the extent of the increase of their size, there was a linear correlation (γ$^2$=0.80, p<0.001, ANOVA), which suggested that an enhancement of q$\_$Tpo/ after high MTX administration can be measured by the increase in their cell size. Taken together, our data demonstrate that the selection of amplified CHO cell clones with enhanced q$\_$Tpo/ can be done upon their increased size and growth pattern. This facilitates the development of highly productive recombinant CHO cell lines.

• Journal of Nutrition and Health
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• 제46권6호
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• pp.503-510
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• 2013

Breast cancer is the most common malignancy in women, both in the developed and developing countries. Anthocyanins are natural coloring of a multitude of foods, such as berries, grapes or cherries. Glycosides of the aglycons delphinidin represent the most abundant anthocyanins in fruits. Delphinidin has recently been reported to inhibit the growth of human tumor cell line. Also, delphinidin is a powerful antioxidant that reportedly exerts beneficial effects in patients with advanced cancer by reducing the level of reactive oxygen species and increasing glutathion peroxidase activity. This study investigates the effects of delphinidin on protein ErbB2, ErbB3 and Akt expressions associated with cell proliferation and Bcl-2, Bax protein associated with cell apoptosis in MDA-MB-231 human breast cancer cell line. MDA-MB-231 cells were cultured with various concentrations (0, 5, 10, and $20{\mu}mol/L$) of delphinidin. Delphinidin inhibited breast cancer cell growth in a dose dependent manner (p < 0.05). ErbB2 and ErbB3 expressions were markdly lower $5{\mu}mol/L$ delphinidin (p < 0.05). In addition, total Akt and phosphorylated Akt levels were decreased dose-dependently in cells treated with delphinidin (p < 0.05). Futher, Bcl-2 levels were dose-dependently decreased and Bax expression was significantly increased in cells treated with delphinidin (p < 0.05). In conclusion, I have shown that delphinidin inhibits cell growth, proliferation and induces apoptosis in MDA-MB-231 human breast cancer cell lines.

• Bulletin of the Korean Chemical Society
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• 제25권9호
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• pp.1297-1298
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• 2004

• 생명과학회지
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• 제34권6호
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• pp.365-376
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• 2024

이 연구는 여러 종류의 암세포주(A-549, AGS, HCT-116, MDA-MB-231 및 U 87-MG)와 정상세포주(MRC-5 및 MSC)에 RNA를 DNA로 전환시킬 수 있는 역전사 효소의 억제 처리 후 세포의 성장에 미치는 영향을 비교 조사하였다. 각 세포주에 efavirenz (EFA) 역전사 효소 억제제를 1주일 동안 처리하였을 때, 세포 성장의 반억제농도(IC₅₀) 값은 암세포주보다 정상세포주에서 더 높은 값을 나타냈다. 결정된 IC₅₀ 값에 따라 15 µM 농도로 EFA를 1주일 동안 처리하였을 때, 역전사 효소 및 말단소립 복원 효소의 활성은 EFA 처리군에서 비처리군에 비하여 유의적으로(p<0.05) 감소하였다. 그러나, 역전사 효소 및 말단소립 복원효소의 활성은 정상세포주에서는 검출되지 않았다. 15 µM EFA를 처리한 후, 암세포주와 정상세포주에서 세포성장율을 비교하였을 때, EFA 처리는 모든 세포의 성장을 억제하였는데, 정상세포주보다 암세포주에서 세포의 성장율이 현저하게(p<0.05) 감소하였다. 또한, 역전사 효소의 억제가 세포의 노화 및 사멸에 미치는 영향을 분석하기 위해 노화 관련 ß-galactosidase 효소의 활성을 분석하였을 때, EFA 처리가 노화관련 효소 활성이 점점 증가하는 것으로 보아, EFA 역전사 효소의 처리는 세포 노화 및 세포 사멸을 유도하는 것을 알 수 있었다. 이상의 결과를 바탕으로, 역전사 효소의 억제는 정상세포보다는 암세포의 성장을 더 억제하는 것을 알 수 있었지만, 항암치료 등에서 응용되기 위해서는 세포에서 역전사 효소의 기능과 역할에 대해서는 좀 더 심도있는 연구가 필요할 것으로 생각된다.

• KSBB Journal
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• 제16권1호
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• pp.30-35
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• 2001

유가식배양과 세라믹 막을 장착한 생물반응기에서 운전인 TCRC 조업을 통해서 Bacillus thuringiensis의 고농도 세포배양을 실시하였다. 유가식 배양에서 B. thuringiensis의 세포 성장은 선형적으로 증가하였고, 이것은 세포성장 모델리의 결과와 잘 맞았다. 낮은 세포 성장속에도 불구하고 유가식 배양동안에 포자형성은 관찰할 수 없었고, 이것은 연속배양의 결과와는 반대였다. 유가식 조업 후에 회분식 배양으로 바꾸면 300 g/L의 포도당 공급 농도를 사용했을 때 2.7$\times$$10^9$ CFU/mL 의 포자농도를 얻었다. 생물반응기내에 세라믹 막을 장착한 TCRC 조업에서 포도당 공급 농도의 영향을 결정하였다. 50 g/L의 포도당 농도를 사용했을 때 TCRC 조업에서 82.5 g-cell/L에 해당하는 최대 세포농도 1.8$\times$$10^{10}$ CFU/mL 를 얻었다. TCRC에서 세포성장은 선형적으로 증가하였고 포도당 농도는 제한되었는데 이것은 세포성장은 모델링의 결과와 잘 일치하였다. 1 g/L의 포도당을 공급한 경우 이외에는 TCRC 조업 동안에 포자형성을 관찰할 수 없었다. 50 g/L의 포도당을 공급한 경우 TCRC조업 후에 회분식 배양으로 전환시키면 1.2$\times$$10^{10}$ CFU/mL 의 포자농도를 얻었고, 이것은 연구된 여러 배양형태 중에 가장 높은 포자농도이다. 이 때 최적의 포도당 공급속도는 0.55 g glucose/h로 공급하였을 때였다.