• Food Science and Biotechnology
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• v.18 no.4
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• pp.971-977
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• 2009

The most abundant tea catechin, epigallocatechin-3-gallate (EGCG), has been reported to inhibit cell proliferation and induce apoptosis in many types of cancer cells. In the present study, effects of EGCG on the growth of oral epithelial cells including CAL-27 oral squamous carcinoma cells and dysplastic oral keratinocytes (DOK) were investigated. EGCG inhibited growth of CAL-27 cells and DOK with $IC_{50}$ of 14.4-21.0 and 5.8-14.2 ${\mu}M$ after 24 and 48 hr incubation, respectively. EGCG was significantly less effective in inhibiting DOK growth. The effects of EGCG, however, were dramatically less pronounced in the presence of superoxide dismutase (SOD) and catalase. Inhibitory effects of EGCG on CAL-27 cell growth were also much less pronounced in the presence of fetal bovine serum (FBS). EGCG induced caspase-3 activation in both CAL-27 and DOK cells in a serum free condition without SOD/catalase; in the presence of 10% FBS and SOD/catalase, EGCG, even at 100 ${\mu}M$, did not affect cell growth. The present results indicate that EGCG inhibited oral cell growth with higher potency to more malignant CAL-27 cells than DOK, and the effects were markedly altered by SOD/catalase and serum content in media.

• The Korean Journal of Mycology
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• v.27 no.1 s.88
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• pp.32-38
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• 1999

A Saprolegnia sp. was isolated from cultured snakehead, Channa argus, and its physiological characteristics were investigated. The optimum temperature, pH and NaCl concentration for mycelial growth of Saprolegnia sp. were $25^{\circ}C$, 6.0 and 0%, respectively. The mycelial growth was increased with the addition of 10 mM phosphate and 10mg/L casamino acid. The essential oils extracted from three plants, Artemisia princeps var. orientalis, Thuja orientalis and Chamaecyparis obtusa have been tested to know whether they inhibit the growth of Saprolegnia sp. at six different oil concentrations(10, 100, 500, 1,000, 1,500 and 2,000 ppm). Essential oil from A. princeps var. orientalis began to inhibite the mycelial growth of Saprolegnia sp. at the concentration more than 10ppm. Using other essential oils from T. orientalis and C. obtusa, those initially inhibited the mycelial growth of Saprolegnia sp. at the concentration over 10 ppm and complate inhibition of mycelial growth was observed at over 500 ppm. The histopathological features of Snakehead infected by Saprolegnia sp. were studied. A club shape of gill lamella epithelial cells was observed in the gill. The mycelial cells were penetrated into muscular tissue, and the accumulation of the ceroid was observed in the liver, spleen and kideny tissue in common. The necrosis of tubular epithelial cells was seen in the liver tissue, parenchymal tissue in the spleen and tubular epithelial cells in the kidney.

• Imaging Science in Dentistry
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• v.30 no.1
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• pp.71-79
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• 2000

Purpose : This study was aimed to evaluate the cell cycle arrest and apoptosis induction after irradiation and epidermal growth factor (EGF) treatment in three human epithelial tumor cell lines (A431, Siha, KB). Materials and Methods: Single irradiation of 2, 5 and 10 Gy was done on three cell lines with 5.38 Gy/min dose rate using Cs-137 irradiator at room temperature. Also, EGF of 10 ng/ml was added immediately after 10 Gy irradiation. Cell growth was evaluated by counting the living cell number using a hemocytometer at 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Cell cycle arrest and apoptosis induction were assayed with the flow cytometry at 8 hours, 12 hours, 1 day, 2 days, 3 days, 4 days and 5 days after irradiation. Results : Growth of irradiated three cell lines were inhibited in proportion to radiation dose. EGF treatment after irradiation showed various results according to cell lines. On all cell lines, G2 arrest was detected after 8 hours and maximized after 12 hours or 1 day. Amount of G2 arrest was positively dose dependent. However, EGF showed no significant change on G2 arrest. G2 arrest was recovered with time at 2 Gy and 5 Gy irradiation. However, at 10 Gy irradiation, G2 arrest was continued. Apoptosis was detected at 10 Gy irradiation. On EGF treated group after irradiation, A431 and Siha cell lines showed slightly increased apoptosis but there was no statistically significant difference. KB cell line showed no marked change of apoptosis induction. Conclusion : Irradiation effects on cell cycle arrest and apoptosis induction in three human epithelial tumor cell lines, however epidermal growth factor doesn't effect on.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.29 no.2
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• pp.131-134
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• 2003

Epithelial-myoepithelial carcinoma(EMC) of the salivary glands is a rare tumor first discribed in 1972. The EMC comprises approximately 1% of all salivary gland tumors. It is characterized by tubular and solid growth pattern with a dual cell population including an inner layer of epithelial cells, which is peripherally bounded by a layer of clear myoepithelial cells. It is demonstrated that tumor with solid slowly growing pattern, generally have a higher frequency of local recurrence. We report a case of parotidic EMC in a 30 years old woman with literature review

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.3
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• pp.177-185
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• 2010

Introduction: Epidermal growth factor receptor (EGFR) is expressed in human epithelial tumors including salivary cancers, and known to be correlated with tumor progression and poor clinical courses in some epithelial tumors. In this study, we determined the therapeutic effect of the anti-EGFR monoclonal antibody Erbitux (C225, cetuximab) in combination with the DNA topoisomerase I inhibitor irinotecan (CPT-11) on human salivary adenoid cystic carcinoma (SACC) cells growing in nude mice. Materials and Methods: At first, immunocytochemical analysis for the expression of EGFR and phosphorylated EGFR (pEGFR) on a human salivary ACC cell line (ACC3). To determine the in vivo effects of Erbitux and CPT-11, nude mice with orthotopic parotid tumors were randomized to receive intraperitoneal Erbitux (1 mg) two times per week, intraperitoneal Irinotecan (50 mg/kg) once per week, Erbitux plus CPT-11, or placebo. (control) Tumor volume and weight were measured. And mechanisms of in vivo activity of Erbitux and/or CPT-11 were determined by immunohistochemical/ immunofluorescent analyses. Results: Immunocytochemical staining of ACC3 demonstrated that EGFR was expressed and phosphorylated. CPT-11 inhibited ACC tumor growth in nude mice. Tumors of mice treated with CPT-11 and CPT-11 plus Erbitux exhibited increased tumor cell apoptosis and decreased microvessel density, which correlated with a decrease in the tumor volume in nude mice. But, CPT-11 seems not to be synergistic with Erbitux in our ACC3 model system. Conclusion: These results suggest that anti-EGFR monoclonal antibody and the DNA topoisomerase I inhibitor will be effective in the treatment of recurred or metastatic lesions of salivary ACC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.2
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• pp.129-134
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• 2001

Since NNK is one of the most abundant tobacco-specific alkaloids and a strong carcinogenic nitrosamine, it has been used for evaluating a potential of carcinogenicity in the animal models. The present study has attempted to examine the potential of carcinogenicity of NNK in human epithelial cells, from which the cell type the most of cancers including oral cancer and nasal cavity cancer are originated. The cellular model used for the study is a human keratinocyte cell system immortalized by Ad12-SV40 hybrid virus. The cellular system has successfully been used for the carcinogenicity studies because of its limitless life span, epithelial morphology and nontumorigenicity. When cells were treated with a variety of NNK concentrations, levels of saturation density and soft agar colony formation were increased in a dose-dependent fashion. Colonies of large cell aggregates were above 5 at the higher doses. The results indicate that exposure of human cells with NNK induced loss of contact inhibition and increases of anchorage independence and cellular adhesion, which are typical characteristics of the neoplatically transformed cells. When cells were exposed with 100uM NNK for 2hr, mRNA levels of IL-1 and PAI-2 were increased in a dose-dependent manner, but expression of TGF- 1 was not affected. While expression of growth regulatory factors were altered with a short-term exposure, there was no alteration of these factors in the NNK-transformed cells. However, mRNA levels of fibronectin were increased both in the short-term treatment and in the transformation. The results suggest that altered expression of extracellular matrix such as fibronectin following short-term exposure might be fixed in the genome and these altered properties be continuously transfered throughout the cell division. Western blot analysis showed a translocation of PKC- from cytosolic fraction to the particulate fraction, indicating a possible role of NNK in the signal transduction pathway. The present study provided an evidence that NNK in the smoking may be associated with epithelial origin cancer such as oral and nasal cavity cancers. In addition, this study suggested that altered expression of extracellular matrix and PKC may play an important role in the carcinogenic mechanism of NNK.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.9
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• pp.4065-4069
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• 2015

Background: Epidermal growth factor-like domain multiple 7 (EGFL7), a secreted protein specifically expressed by endothelial cells during embryogenesis, recently was identified as a critical gene in tumor metastasis. Epithelial-mesenchymal transition (EMT) was found to be closely related with tumor progression. Accordingly, it is important to investigate the migration and EMT change after knock-down of EGFL7 gene expression in human pancreatic cancer cells. Materials and Methods: EGFL7 expression was firstly testified in 4 pancreatic cancer cell lines by real-time polymerase chain reaction (Real-time PCR) and western blot, and the highest expression of EGFL7 was found in PANC-1 cell line. Then, PANC-1 cells transfected with small interference RNA (siRNA) of EGFL7 using plasmid vector were named si-PANC-1, while transfected with negative control plasmid vector were called NC-PANC-1. Transwell assay was used to analyze the migration of PANC-1 cells. Real-time PCR and western blotting were used to detect the expression change of EGFL7 gene, EMT markers like E-Cadherin, N-Cadherin, Vimentin, Fibronectin and transcription factors like snail, slug in PANC-1, NCPANC-1, and si-PANC-1 cells, respectively. Results: After successful plasmid transfection, EGFL7 gene were dramatically knock-down by RNA interference in si-PANC-1 group. Meanwhile, migration ability decreased significantly, compared with PANC-1 and NC-PANC-1 group. Meanwhile, the expression of epithelial phenotype marker E-Cadherin increased and that of mesenchymal phenotype markers N-Cadherin, Vimentin, Fibronectin dramatically decreased in si-PANC-1 group, indicating a reversion of EMT. Also, transcription factors snail and slug decreased significantly after RNA interference. Conclusions: Current study suggested that highly-expressed EGFL7 promotes migration of PANC-1 cells and acts through transcription factors snail and slug to induce EMT, and further study is needed to confirm this issue.

• Journal of the korean academy of Pediatric Dentistry
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• v.38 no.4
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• pp.399-406
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• 2011

Traumatic injury on tooth occurs frequently among trauma patients, and mainly occurs on tooth with premature roots which influences pulp tissue, periodontal ligament, alveolar bone, and Hertwig's epithelial root sheath. According to the degree of trauma, a number of kinds of healing process can be observed, such as complete re-vascularization of pulp, root canal obliteration, growth suspension of root apex, and invasion of alveolar bone into root canal, and there can be some complications such as necrotic change of inflammatory root resorption and partial pulp necrosis due to pulp necrosis toward complete necrosis. In this clinical case, 3 patients who had traumatic injury showed root growth suspension and alveolar bone invasion into root canal due to proliferation of periodontal ligament cell and osteocyte at the base of extraction socket into pulp chamber because of the injury on Hertwig's epithelial root sheath. If intrusion of alveolar bone into root canal due to injury on Hertwig's epithelial root sheath after having traumatic injury doesn't show any complication, the pulp may be considered to have normal vitality and doesn't need any further treatment, therefore differential diagnosis is very necessary. However, it may be accompanied with suspension of root growth, therefore, additional trauma during the treatment of injured tooth should not be applied.

• Journal of Ginseng Research
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• v.45 no.1
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• pp.134-148
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• 2021

Background: Lung cancer has a high incidence worldwide, and most lung cancer-associated deaths are attributable to cancer metastasis. Although several medicinal properties of Panax ginseng Meyer have been reported, the effect of ginsenosides Rk1 and Rg5 on epithelial-mesenchymal transition (EMT) stimulated by transforming growth factor beta 1 (TGF-β1) and self-renewal in A549 cells is relatively unknown. Methods: We treated TGF-β1 or alternatively Rk1 and Rg5 in A549 cells. We used western blot analysis, real-time polymerase chain reaction (qPCR), wound healing assay, Matrigel invasion assay, and anoikis assays to determine the effect of Rk1 and Rg5 on TGF-mediated EMT in lung cancer cell. In addition, we performed tumorsphere formation assays and real-time PCR to evaluate the stem-like properties. Results: EMT is induced by TGF-β1 in A549 cells causing the development of cancer stem-like features. Expression of E-cadherin, an epithelial marker, decreased and an increase in vimentin expression was noted. Cell mobility, invasiveness, and anoikis resistance were enhanced with TGF-β1 treatment. In addition, the expression of stem cell markers, CD44, and CD133, was also increased. Treatment with Rk1 and Rg5 suppressed EMT by TGF-β1 and the development of stemness in a dose-dependent manner. Additionally, Rk1 and Rg5 markedly suppressed TGF-β1-induced metalloproteinase-2/9 (MMP2/9) activity, and activation of Smad2/3 and nuclear factor kappa B/extra-cellular signal regulated kinases (NF-kB/ERK) pathways in lung cancer cells. Conclusions: Rk1 and Rg5 regulate the EMT inducing TGF-β1 by suppressing the Smad and NF-κB/ERK pathways (non-Smad pathway).

• Proceedings of the Korean Nuclear Society Conference
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• 2005.05a
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• pp.1002-1003
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• 2005