• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.123-129
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• 1995

장차 세포증식과 분화의 전환에 있어서 세포주기의 구성요소들과 Rb 사이의 상호관계 및 세포주기의 조절과 DNA 손상에 대한 p53의 역할을 함께 상세하게 �P혀야 한다. 형질전환된 경우에는 p16과 p21을 포함하여 관련된 CDI들에 의한 cyclin과 CDK의 복합체의 조절에 있어서 중요한 변화들을 야기시키므로 CDI들의 불활성과 발암현상과의 정확한 인과관계를 �P혀내야 한다. 발아 또는 분열효모균에서 Sic 1과 Rum 1과 같은 cyclin-CDK의 중요한 조절인자들이 확인되었는데, 포유동물에 있어서 이러한 단백들에 대한 대응물들을 기대해보며, 체크포인트와 세포사망기전 및 암세포들에 있어서 탈조절에 대한 이해가 새로운 항암치료제 개발에 중요하다고 생각된다.

• Korean Journal of Food Science and Technology
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• v.30 no.6
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• pp.1470-1475
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• 1998

Two kinds of Korean rice-wine (Yakju) with different process and ingredients, and Japanese rice-wine (Sake) were chosen for this study, and throughly dried and solubilized in water or cell culture medium. In vitro cytotoxicity assays of the solubilized wine solids exhibited that maximum dilution factors for inhibition of B 16BL6 mouse melanoma cell growth were 16X for herbal medicine-added rice-wine (Korean rice-wine I) and typical Korean rice-wine (Korean rice-wine II), and 8X for Japanese rice-wine. Their cytotoxic effects on HRT18 human colon adenocarcinoma cells were even lower than those on B16BL6 cells. The morphology of the tumor cells were changed by addition of the solubilized wine solids. Inhibitory effect of the rice-wine on in vivo tumor growth and metastasis were monitored after implantation of B16BL6 cells into C57BL/6 mice with daily feeding the solubilized wine solids. Compared to non-fed control groups, B16BL6 tumor growth and metastasis to lung were clearly inhibited by feeding the wine solids, in order of Korean rice-wine I > Korean rice-wine II > Japanese rice-wine. The data of in vitro cytotoxicity and the cell shape changes indicate that the inhibitory effect of tumor progression may be attributed to tumor cell differentiation or immune stimulation induced by certain components in the rice-wine, rather than direct cytotoxicity of the components.

• Journal of Life Science
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• v.9 no.2
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• pp.160-168
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• 1999

Butyrate is one of the short-chain fatty acids that are present in the colon of mammals in millimolar concentration as a result of microbial anaerobic fermentation of dietary fiber, undigested starch, and proteins. In this study, sodium butyrate was examined in HT29 cell, human colonic cancer cell line, on cell viability, alkaline phosphatase activity, PLC-${\gamma}$1 expression and complex sphingolipid biosynthesis. Treatment with butyrate showed that the decrease of cell adhesion and viability was time-dependent. Sodium butyrate also induced to increase the activity of alkaline phosphatase which is a differentiation marker enzyme and decrease the expression of PLC-${\gamma}$1. Biosynthesis of sphingomyelin and galactosylceramide by butyrate treatment were decreased so fast but ceramide was increased 680dpm/mg protein% more than untreated group on first day and then decreased fast. In addition, acid ceramidase and neutral ceramidase activity were inhibited early stage by sodium butyrate. These results suggest that sodium butyrate causes cell differentiation or cell growth arrest of HT29 cell accompanied by early increase of ceramide content and alkaline phosphatase activity and decrease of galactosylceramide content and PLC-r1 expression.

• Journal of Life Science
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• v.21 no.5
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• pp.631-646
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• 2011

Mesenchymal stem cells (MSC) are multipotent and can be isolated from diverse human tissues including bone marrow, fat, placenta, dental pulp, synovium, tonsil, and the thymus. They function as regulators of tissue homeostasis. Because of their various advantages such as plasticity, easy isolation and manipulation, chemotaxis to cancer, and immune regulatory function, MSCs have been considered to be a potent cell source for regenerative medicine, cancer treatment and other cell based therapy such as GVHD. However, relating to its supportive feature for surrounding cell and tissue, it has been frequently reported that MSCs accelerate tumor growth by modulating cancer microenvironment through promoting angiogenesis, secreting growth factors, and suppressing anti-tumorigenic immune reaction. Thus, clinical application of MSCs has been limited. To understand the underlying mechanism which modulates MSCs to function as tumor supportive cells, we co-cultured human adipose tissue derived mesenchymal stem cells (ASC) with cancer cell lines H460 and U87MG. Then, expression data of ASCs co-cultured with cancer cells and cultured alone were obtained via microarray. Comparative expression analysis was carried out using DAVID (Database for Annotation, Visualization and Integrated Discovery) and PANTHER (Protein ANalysis THrough Evolutionary Relationships) in divers aspects including biological process, molecular function, cellular component, protein class, disease, tissue expression, and signal pathway. We found that cancer cells alter the expression profile of MSCs to cancer associated fibroblast like cells by modulating its energy metabolism, stemness, cell structure components, and paracrine effect in a variety of levels. These findings will improve the clinical efficacy and safety of MSCs based cell therapy.

• Korean Journal of Medicinal Crop Science
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• v.12 no.3
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• pp.243-248
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• 2004

Essential oils from Needl Juniperrus seed and trunk (Juniperrus rigida Sieb.) and Olibanum resin (Boswellia carteii Birew) were extracted by a supercritical fluid extraction system (SFE) and immune activity of each essential oils were observed. The immune activities of each essential oil were compared. Essential oil from Olibanum resin enhanced the growth of human immune T cell up to 1.33 times, compared to control group. Each essential oils showed the potent inhibitory effect on the human cancer cell lines, and increased the secretion of cytokines, IL-6 and $TNF-{\alpha}$ from human B cell as well as the growth of human immune cells.

• Korean Journal of Food Science and Technology
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• v.48 no.4
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• pp.378-383
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• 2016

The glasswort is an edible halophyte demonstrating various physiological effects including anti-inflammatory activity. In the present study, the effects of glasswort extracts on inflammatory events and interactions of THP-1 monocytes with intestinal epithelial cells were investigated. Five solvent fractions, including the ethylether fraction (Fr.E), were prepared from a 70% methanol extract of glasswort. THP-1 monocytes underwent differentiation by phorbol 12-myristate 13-acetate treatment and were then activated by lipopolysaccharide (LPS), which induced cyclooxygenase (COX)-2 expression. None of the glasswort fractions tested alone induced COX-2 in differentiated THP-1 cells. Fr.E, however, enhanced LPS-induced COX-2 expression in differentiated THP-1 cells. Culture media of THP-1 cells treated with each fraction stimulated the growth of normal intestinal INT-407 cells more prominently than that of HT-29 colon cancer cells. COX-2 expression in HT-29 cells was inhibited when the cells were exposed to the THP-1 culture medium treated with Fr.E. Thus, glasswort could modulate the interaction between immune cells and intestinal cells.

• Korean Journal of Bronchoesophagology
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• v.5 no.2
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• pp.119-126
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• 1999

Objectives : To analyze the effect of retinoids on the differentiation in HNSCC xenografts. Materials and Methods : RA (20mg/kg) or 13-cis-RA (60mg/kg) was orally administered once in a day for 30 days in the xenograft model we prepared using athymic nude mice with AMCHN-4 and -6. We carried out H & E staining and immunohistochemical staining with the monoclonal antibody against involucrin and cytokeratin 10. Results : Both RA and 13-cis-RA were found to suppress the differentiation of AMC-HN-4. Interestingly, RA enhanced the differentiation of AMC-HN-6, although 13-cis RA did not exhibit any effect on the differentiation. These results suggest that in vivo effect of retinoids on the HNSCC growth and differentiation might be various. Retinoids-induced P450 in AMC-HN-6 might be one of the mechanisms to explain the reason why the retinoids exhibit various functions in the HNSCC.

• Tuberculosis and Respiratory Diseases
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• v.40 no.1
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• pp.23-28
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• 1993

Background: Since an important component of carcinogenesis is unregulated growth, many investigators have reported the methods to detect cell proliferation in tissues including PCNA. PCNA is a 36 Kd intranuclear polypeptide and plays a critical role in cell proliferation. Thus progressive dysregulation of proliferation during carcinogenesis can be directly visualized in the paraffin embedded tissue using immunohistochemistry for PCNA which has an advantage of simplicity and maintenance of tissue architecture. The heterogeneity of PCNA expression is known to be related with proliferating fraction, histologic grade, DNA ploidy, and susceptibility of anticancer drugs, etc. We analyzed the biologic significance of the expression of PCNA in lung cancer tissues. Method: 43 lung cancer tissues, which were resected by surgery and were embedded in paraffin, were stained immunohistochemically by one hour MicroProbe System and the results were corelated with cell type, stage, site and survival. Result: 1) Suamous cell type showed high positivity (89%) than in adenocarcinoma (54%). 2) No significant difference related to tumor stage was noticed. 3) No significant difference between primary site and metastatic site was noticed. 4) No significant difference in 12-month survival between positive group and negative group was noticed. Conclusion: From this study, we concluded that imunohistochemistry for PCNA expression of routinely processed tissue is a simple technique for the assessment of proliferation in non-small cell lung cancer. Whether the labelling index has an independent prognostic value and deserves special attention in pathobiological evaluation in lung cancer remains to be investigated from large series with longer follow-up and to be correlated with multiple biological markers.

• Journal of Life Science
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• v.16 no.3 s.76
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• pp.433-441
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• 2006

Polyamines are essential for the normal cell growth and differentiation. They are also known to have paradoxical dual effects on cell proliferation. In this paper we show that the excess amount of polyamines induces apoptosis through the modulation of calcium signaling in LNCaP human prostate cancer cells. Polyamines, particularly spermidine and spermine, stimulated cell proliferation at a lower concentration (under 10 ${\mu}M$), but it inhibited cell viability at a higher concentration (40 ${\mu}M$). The levels of intracellular $Ca^{2+}$ concentration were increased only at a high concentration of polyamines treatment without any noticeable changes at lower concentrations. Nifedipine did not alter the increase of polyamine-induced $Ca^{2+}$ levels, but flufenamic acid totally abolished the increase of intracellular $Ca^{2+}$ levels. These results mean that polyamines induce $Ca^{2+}$ influx from the surroundings through nonselective cation channels on the cell membrane. The expression of Bcl-2 protein was almost completely blocked, but the level of Bax protein was increased dramatically in the cells treated with high concentration of polyamine. The present study shows that polyamines at a high concentration induce apoptosis through the modulation of intracellular calcium signaling. The increase of intracellular calcium level induced by polyamines, was possibly a result from the extracellular calcium influx through the nonselective cation channels.

• Journal of Life Science
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• v.22 no.1
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• pp.55-61
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• 2012

Akt is known to play an important role in cell proliferation and differentiation, and is also over-expressed in several types of cancer cells. In this study, we explored the anti-proliferative effects of selenium in HT-29 colon cancer cells, mediated through effects on Akt and COX-2. Selenium treatments at different concentrations and for different durations inhibited proliferation of HT-29 colon cancer cells and increased apoptotic cell death. Selenium treatment decreased Akt phosphorylation and COX-2 expression. Treatment with LY294002 (an Akt inhibitor) decreased proliferation of HT-29 cells, while a combined treatment with LY294002 and selenium resulted in even further decreases in cell proliferation. Inactivation of Akt by Akt siRNA treatment abolished these inhibitory effects on cell growth. COX-2 expression decreased in Akt transfected cells compared to non-transfected cells. These results suggest that selenium induced both anti-proliferative and apoptotic effects by inhibiting Akt phosphorylation and COX-2 expression. Selenium treatment also appeared to induce synergistic anti-proliferative effects by inhibition of Akt in HT-29 colon cancer cells.