• 한국환경보건학회지
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• 제22권2호
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• pp.10-18
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• 1996

Experiments were carried out to find the possibility of an economic production of single cell protein(SCP) in mixed culture by Cellulomonas sp. KL-6 and a second organism. The second organism, strain LI-10, was isolated from the large intestines of a mouse. 1. When these strains were mixed, cell growth and carboxymethyl cellulase (CMCase) activity were increased to about 63% and 161%, respectively compared with that of single culture of strain KL-6. We found the mixed culture as a proper method of degradation of cellulose in our study. 2. Strain LI-10 was identified as E. coli. 3. This strain produced trace amounts of cellobiose, but glucose was not found in detectable amounts in the filter paper(FP) medium. 4. $CaCO_3$ injected in the medium at the ratio of 0.1% not only enhanced cell growth but also was effective as an acid neutralizing agent. 5. When this organism was cultured under the optimal medium (glucose 0.1%, $NH_4Cl$ 0.1%, yeast extract 2.0%, $KH_2PO_4$ 0.1%, KCl 0.05%, pH 7.2 and a temperature 30$\circ$C) for 5 days, a cell mass produced 1.18 g/l. The results showed the increase of cell mass up to 300% compared to 0.28 g/l produced in CMC medium.

• 한국동물학회지
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• 제32권4호
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• pp.404-411
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• 1989

In this study, we attempted to determine the precise patterns of protein synthesis during the second cleavage in mouse. F1 hybrid 2-cell embryos showing a highly synchronized cell cycle and outbreed ICR strain 2-cell embryos were used. The patterns of protein synthesis during the second cleavage showed the sequential changes in the F1 hybrid and ICR strain 2-cell embryos. Moreover, we examined the effects of mitotic and transcriptional inhibitors such as colcemid and a-amanitin on the protein synthesis in the late 2-cell embryos of ICR strain. Treatment of colcemid (0.1mg/ml) blocked the second cleavage, but did not affect on the change of protein synthesis. However, treatment of a-amanitin induced the synthesis of two set of polypeptides without affecting on synthesis of other proteins and cleavage. It thus seems that the appearance of a-amanitin-sensitive proteins may be not involved in the second cleavage. Therefore, these results indicate that the second cell cycle in mouse embryos appears to be regulated at post transcriptional level, presumably independent on the expression of embryonic genome. 본 연구는 생쥐 배아의 2세포기 분열과정중 단백질 합성양상과 단백질합성에 미치는 colcemid와 $\alpha$-amanitin의 영향을 조사하였다 이를 위하여 체내 수정된 ICR strain의 2세포기 배아와 매우 일치된 초기배아 분열양상을 보여주는 체외 수정된 F1 (C57BL x CBA) hybrid 2세포기 배아를 사용하였다. 두 종류의 2세포기 배아에서 단백질 합성은 분열단계에 따라서 매우 일치된 변화를 보여 주었다. 또한 유사분열 억제제인 colcemid (0.1mg/ml)의 처리는 2세포기 배아분열을 억제하였으나, 단백질 합성에는 아무런 변화를 주지 못하였다. 그리고 후기 2세포기 배아에 전사 억제제인 a-amanitin (100mg/ml)을 처리하였을 때 세포분열이나 다른 단백질의 합성에는 아무런 영향이 없이 단지 두개의 단백질의 합성만을 유도하였다. 이는 아마도 a-amanitin의 stress효과에 기인하는 것으로 추측된다. 따라서 생쥐 2세포기 배아의 분열과정은 배아게놈의 유전자 발현과는 무관하게 이미 합성되어 존재하는 mRNA에 의하여 조절되는 것으로 사료된다.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1281-1284
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• 2012

Background: Platinum-hased chemotherapy for advanced non-small cell lung cancer (NSCLC) is still considered the first choice, presenting a modest survival advantage. However, the patients eventually experience disease progression and require second-line therapy. While there are reliable predictors to identify patients receiving first-line chemotherapy, very little knowledge is available about the prognostic factors in patients who receive second-line treatments. The present study was therefore performed. Methods: We retrospectively reviewed 107 patients receiving second-line treatments from August 2002 to March 2012 in the Dicle University, School of Medicine, Department of Medical Oncology. Fourteen potential prognostic variables were chosen for analysis in this study. Univariate and multivariate analyses were conducted to identify prognostic factors associated with survival. Result: The results of univariate analysis for overall survival (OS) were identified to have prognostic significance: performance status (PS), stage, response to first-line chemotherapy response to second-line chemotherapy and number of metastasis. PS, diabetes mellitus (DM), response to first-line chemotherapy and response to second-line chemotherapy were identified to have prognostic significance for progression-free survival (PFS). Multivariate analysis showed that PS, response to first-line chemotherapy and response to second-line chemotherapy were considered independent prognostic factors for OS. Furthermore, PS and response to second-line chemotherapy were considered independent prognostic factors for PFS. Conclusion: In conclusion, PS, response to first and second-line chemotherapy were identified as important prognostic factors for OS in advanced NSCLC patients who were undergoing second-line palliative treatment. Furthermore, PS and response to second-line chemotherapy were considered independent prognostic factors for PFS. It may be concluded that these findings may facilitate pretreatment prediction of survival and can be used for selecting patients for the correct choice of treatment.

• 한국정밀공학회:학술대회논문집
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• 한국정밀공학회 2010년도 추계학술대회 논문집
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• pp.991-992
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• 2010

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3757-3761
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• 2012

Objective: Crocin has been proposed as a promising candidate for cancer chemoprevention. The purpose of this investigation was to investigate the chemopreventive action and the possible mechanisms of crocin against human colon cancer cells in vitro. Methods: Cell proliferation was examined using MTT assay and the cell cycle distribution fractions were analyzed using fow cytometric analysis after propidium iodide staining. Apoptosis was detected using theTUNEL Apoptosis Detection Kit with laser scanning confocal microscope. DNA damage was assessed using the alkaline single-cell gel electrophoresis assay, while expression levels of p53, cdk2, cyclinA and P21 were examined by Western blot analysis. Results: Treatment of SW480 cells with crocetin (0.2, 0.4, 0.8 mmol/L) for 48 h signifcantly inhibited their proliferation in a concentration-dependent manner. Crocetin (0.8 mmol/L) signifcantly induced cell cycle arrest through p53-independent mechanisms accompanied by P21 induction. Crocetin (0.8 mmol/L) caused cytotoxicity in the SW480 cells by enhancing apoptosis and decreasing DNA repair capacity in a time-dependent manner. Conclusions: This report provides evidence that crocetin is a potential anticancer agent, which may be used as a chemotherapeutic drug.

• Molecules and Cells
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• 제41권3호
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• pp.188-197
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• 2018

Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial-mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker expression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was activated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.

• Asian Pacific Journal of Cancer Prevention
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• 제14권5호
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• pp.3001-3003
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• 2013

Objective: Spleen tyrosine kinase (Syk) is closely related to tumor invasion and metastasis, and has been shown to have potential inhibitory effects in tumors. In this study, we constructed a eukaryotic expression vector for Syk and analyzed its effects on invasive ability of the A549 non-small cell lung cancer cell line in vitro. Methods: A fragment of Syk was obtained by RT-PCR from human lung cancer cells and cloned into the expression vector pLNCXSyk. After restriction endonuclease digestion, PCR and DNA sequencing confirmation, the recombinant Syk expression plasmid was transfected into A549 human lung cancer cells using lipofectamine protocols. After selection, the cells stably expressed Syk. Detection of Syk expression of the cells by RT-PCR, and invasive ability were examined. Results: The eukaryotic expression plamid pLNCXSyk was constructed and expressed stably in the A549 human lung cancer cells. The RT-PCR results showed that Syk mRNA expression was upregulated significantly (P<0.05). Lower invasion through a basal membrane were apparent after transfection (P<0.05). Conclusions: A eukaryotic expression plasmid to cause Syk expression in lung cancer cells can obviously inhibit their invasive ability in vitro.

• BMB Reports
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• 제44권8호
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• pp.547-552
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• 2011

MED19 is a member of the Mediator that plays a key role in the activation and repression of signal transduction or the regulation of transcription in carcinomas. To tested the functional role of MED19 in human prostate cancer, we downregulated MED19 expression in prostate cancer cells (PC-3 and DU145) by lentivirus-mediated short hairpin (shRNA), and analyzed the effect of inhibition of MED19 on prostate cancer cell proliferation and tumorigenesis. The in vitro prostate cancer cell proliferation, colony formation, and in vivo tumor growth in nude mice xenografts was significantly reduced after the downregulation of MED19. Knockdown of MED19 caused S-phase arrest and induced apoptosis via modulation of Bid and Caspase 7. It was suggested that MED19 serves as a novel proliferation regulator that promotes growth of prostate cancer cells.

• Biomolecules & Therapeutics
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• 제26권2호
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• pp.121-129
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• 2018

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX-1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.

• BMB Reports
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• 제52권5호
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• pp.312-317
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• 2019

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality worldwide. MiR-371 has recently emerged as an important regulator in tumorigenesis, and may serve as a biomarker for malignant tumors. We transfected miR-371 or its inhibitor in two human HCC cell lines, then used 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, soft agar colony formation, and transwell migration assays to evaluate the effects on cell proliferation, migration, and invasion. We found that miR-371 was positively correlated with HCC metastasis and poor prognosis in the inflicted patients, and the high expression of miR-371 was promoted, whereas a low level of miR-371 depressed cell proliferation and invasion. We found PTEN to be a direct target of miR-371. The overexpression or knockdown of PTEN exhibited the opposite effects from those of miR-371 on cell proliferation and migration. Our study demonstrates that miR-371 promotes proliferation and metastasis in HCC by targeting PTEN.