• Bulletin of Food Technology
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• v.16 no.4
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• pp.93-105
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• 2003

• Animal cells and systems
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• v.2 no.1
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• pp.117-122
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• 1998

D-raf, a Drosophila homolog of the human c-raf-1, is known as a signal transducer in cell proliferation and differentiation. A previous study found that the D-raf gene expression is regulated by the DNA replication-related element (DRE)/DRE-binding factor (DREF) system. In this study, we found the sequences homologous to transcription factor C/EBP, MyoD, STAT and Myc recognition sites in the D-raf promoter. We have generated various base substitutional mutations in these recognition sites and subsequently examined their effects on D-raf promoter activity through transient CAT assays in Kc cells with reporter plasmids p5'-878DrafCAT carrying the mutations in these binding sites. Through gel mobility shift assay using nuclear extracts of Kc cells, we detected factors binding to these recognition sites. Our results show that transcription factor C/EBP, STAT and Myc binding sites in D-raf promoter region play a positive role in transcriptional regulation of the D-raf gene and the Myo D binding site plays a negative role.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.6
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• pp.1441-1447
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• 2003

The purpose of this research was to investigate the effects of Chungjokupye-tang(CJKPT) on the anti-carcinogenic action. The cell viability of mouse spienocytes and thymocytes were enhanced by the addition of CJKPT. CJKPT were increased of splenic and thymic T lymphocytes, such as T/sub H/ cells were markedly increased by the treatment of CJKPT in vivo. CJKPT treatment induced the apoptotic cell death of Jurkat and HL60 leukemia cells. CJKPT reduced mitochondrial transmembrane potential and increased the expression of ICE, c-myc and p53 gene in Molt-4cells dose dependant manner. These results suggest that CJKPT have an anti-carcinogenic action via immunoregulatory mechanism.

• Microbiology and Biotechnology Letters
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• v.22 no.4
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• pp.347-352
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• 1994

Cytotoxic test was performed by SRB assay on human epidermoid carcinoma HEp-2 cell line for screening the soil microorganism, secreting anticancer agent. One microorganism was selected among two thousand microorganisms for its highest cytotoxicity. And this microorganism was identified with Streptomyces species after performing of diaminopimeric acid and reducing sugar analysis of cell wall and analysing the cultural characteristics and named Streptomyces sp. SM 1119. The effect of anticancer agent in SM 1119 culture extract on the cell cycle was studied by using GG$_{o}$ synchronized NIH 3T3 cells. The extract inhibited the serum stimulation of GG$_{o}$ NIH 3T3 cell only within 1 hour after serum stimulation but not after 6 hours. The extract also reduced the amount of c-myc mRNA in Colo 320 cell. These results suggest that the anticancer agent in the extract inhibits the progression of cell cycle very early stages, probably from G$_{0}$ to G$_{1}$.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.162-162
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• 2004

• BMB Reports
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• v.52 no.1
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• pp.70-85
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• 2019

Reduction of insulin/insulin-like growth factor 1 (IGF1) signaling (IIS) extends the lifespan of various species. So far, several longevity mouse models have been developed containing mutations related to growth signaling deficiency by targeting growth hormone (GH), IGF1, IGF1 receptor, insulin receptor, and insulin receptor substrate. In addition, p70 ribosomal protein S6 kinase 1 (S6K1) knockout leads to lifespan extension. S6K1 encodes an important kinase in the regulation of cell growth. S6K1 is regulated by mechanistic target of rapamycin (mTOR) complex 1. The v-myc myelocytomatosis viral oncogene homolog (MYC)-deficient mice also exhibits a longevity phenotype. The gene expression profiles of these mice models have been measured to identify their longevity mechanisms. Here, we summarize our knowledge of long-lived mouse models related to growth and discuss phenotypic characteristics, including organ-specific gene expression patterns.

• Proceedings of the Zoological Society Korea Conference
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• 1994.10a
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• pp.162.1-162
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• 1994

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1996.04a
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• pp.44.1-44
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• 1996

No Abstract, See Full Text

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.3
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• pp.443-452
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• 1994

This study describes the effects of novel1, 25-dihydroxyvitamin D$_3$ analong[1,25(OH)$_2$-16ene-23yne-26, 27-F6-D$_3$] on proliferation of the human histiocytic lymphoma cell line U937 in vitro. We also examined the expression of c-myc oncogene in U937 cells was apparently inhibited to 62% and 87% of the control level after 4 days in the presence of 10-8M and 10-7 M of this analog, respectively. This compound morpholgically and functionally differentiated U937 cells to nonocyte-macrophage phenotype showing the increase of adherence ability to surface and a decrease of N/C ratio in Giemsa staining . Especially, nonspecific esterase activity which is a marker of cell differentiation to monocyte-macrophage was positive, and production of the positive stained cells increased in a dose dependent fashion . The expression of c-myc oncogene by 1, 25(OH)$_2$D$_3$ analog(10-7 M) was reduced by 60% at the mRNA level as determined by Northern blotting. The effects of this novel analog on cell proliferation and cell differentiation may open op new therapeutic strategies for human disorders such as psoriassis and may provide a tool to understand the mechanism of action of vitamin D$_3$ seco-steroids in malignancy.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.60-67
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• 2000

Background: Microsatellites are short-tandem repeated uncleotide sequences present throughout the human genome. Alterations of microsatellites have been termed microsatellite instability(MI). It has been generally known that microsatellite instability detected in hereditary non-polyposis colorectal cancer (HNPCC) reflects genetic instability that is caused by impairments of DNA mismatch repair system regarding as a novel tumorigenic mechanism. A number of studies reported that MI occurred at varying frequencies in non-small cell lung carcinoma (NSCLC). However It has been unproven whether MI could be a useful market of genetic instability and have a clinical significance in NSCLC. Material and Method : We have examined whether MI can be observed in thirty NCSLC using polymerase chain reaction whether such alterations are associated with other molecular changes such as p53, K-ras and c-myc oncoproteins expression detected by immunohistochemical stain,. Result: MI(+) was observed in 16.6%(5/30) and MI(-) was 83.3% (25/30) Average age was 50$\pm$7.5 year-old in MI(+) group and 57$\pm$6.6 year-old in MI(-) group. Two year survival rate in MI(=) group (20% 1/5) was worse than MI(-) group (64% 16/25) with a statistic difference. (P=0.04) The positive rate of K-ras oncoprotein expression and simultaneous expression of 2 or 3 oncoproteins expression were higher in MI(+) group than MI(-) group with a statistic difference(P=0.05, P=0.01) Conclusion: From, these results the authors can conclude that MI is found in some NSCLC and it may be a novel tumorigenic mechanism in some NSCLC. We also conclude that MI could be used as another poor prognostic factor in NSCLS.