• Communications of the Korean Mathematical Society
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• v.38 no.4
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• pp.1299-1307
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• 2023

In this paper, we attempt to study several topological properties for the function space H(X), space of self-homeomorphisms on a metric space endowed with the regular topology. We investigate its metrizability and countability and prove their coincidence at X compact. Furthermore, we prove that the space H(X) endowed with the regular topology is a topological group when X is a metric, almost P-space. Moreover, we prove that the homeomorphism spaces of increasing and decreasing functions on ℝ under regular topology are open subspaces of H(ℝ) and are homeomorphic.

• Proceedings of the Korean Society of Precision Engineering Conference
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• 2012.05a
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• pp.1299-1300
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• 2012

• Proceedings of the Korean Society of Precision Engineering Conference
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• 2011.06a
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• pp.1299-1300
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• 2011

• Biomolecules & Therapeutics
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• v.19 no.4
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• pp.411-418
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• 2011

Ginsenoside Rp1 (G-Rp1) is a novel ginseng saponin derivative with anti-tumor activity. However, the biochemical and molecular mechanisms of G-Rp1 on anti-tumor activity are not fully understood. In the present study, we report that G-Rp1 inhibits lung cancer cell proliferation, migration and adhesion in p53 wild-type A549 and p53-defi cient H1299 cells. Anti-proliferative activity of G-Rp1 in lung cancer cells is mediated by enhanced nuclear localization of cyclin-dependent kinase inhibitors including $p27^{Kip1}$ and $p21^{WAF1/Cip1}$, and subsequent inhibition of pRb phosphorylation. We also show that these anti-tumor activities of G-Rp1 in both A549 and H1299 cells appear to be mediated by suppression of mitogenic signaling pathways such as ERK, Akt and $p70^{S6K}$. Taken together, these findings suggest further development and evaluation of G-Rp1 for the treatment of lung cancers with mutated p53 as well as wild-type p53.

• Microbiology and Biotechnology Letters
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• v.32 no.1
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• pp.72-77
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• 2004

Previously, we synthesized a novel Cyclin-dependent kinase inhibitor, MCS-5A. Also, we investigated the involvement of cell cycle regulatory events during MCS-5A-mediated apoptosis in HL-60(+p16/-p53) cells with up-regulation of p16 protein expression. In contrast, apoptosis was not observed in A549(-p16/+p53) cells. Therefore we propose that $p16^{INK4A}$ is a key enzyme for inducing apoptosis. In the present studies, we have explored the mechanism of $p16^{INK4A}$ -mediated cytotoxicity and the role of p16.sup INK4A/ overexpression in the induction of apoptosis in human tumor cells. The tumor suppressor gene $p16^{INK4A}$ is known as a cyclin-dependent kinase inhibitor (CKI) and cell cycle regulator. We expressed wild type $p16^{INK4A}$ in pcDNA3.1 vector and then transfected into non-small cell lung cancer (NSCLC) cell expressing different statue of p16$^{INK4A}$, p53 gene〔A549(-p16/+p53), H1299(-p16/-p53) and HeLa(+pl6/+p53) cell line〕. TUNEL assay (including propidium iodide staining following transfection of these cell line with pcDNA3.1-pl6) indicate that p16$^{INK4A}$-mediated cytotoxicity was associated with apoptosis. This is supported by studies demonstrating an induction of caspase 3 cleavage due to the transfection of A549, H1299 and HeLa cells with pcDNA3.1-pl6. These results suggest that p16$^{INK4A}$ has a new function of inducing apoptosis which is not related with the function of tumor suppressor gene p53.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.1
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• pp.44-51
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• 2016

The aim of the study was to investigate the antioxidant content and activities of ethanol extract of the edible flower Dianthus chinensis L. (DCE) as well as its inhibitory activities against nitric oxide (NO) production in macrophages and growth and adhesion of human cancer cells. The total polyphenol, flavonoid, and carotenoid levels of DCE were 19.0 mg gallic acid equivalent/g, 65.7 mg quercetin equivalent/g, and $95.0{\mu}g/g$, respectively. The 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and ferric reducing antioxidant power of DCE at a concentration of $1,000{\mu}g/mL$ were 44% and 51%, respectively. In lipopolysaccharide-treated RAW 264.7 macrophages, treatment with DCE at concentrations of 500 and $1,000{\mu}g/mL$ resulted in significantly reduced NO levels (to 7~23% of the control). In H1299 human lung carcinoma cells and HCT116 human colorectal carcinoma cells, treatment with DCE at concentrations of 250, 500, and $1,000{\mu}g/mL$ resulted in dose-dependent growth inhibition. DCE was also effective in inhibiting adhesion of both H1299 cells (to 55% of the control at concentration of $1,000{\mu}g/mL$) and HCT116 (to 26~40% of the control at concentrations of 250, 500, and $1,000{\mu}g/mL$). These results suggest that DCE exerts antioxidant, anti-inflammatory, and anti-cancer activities in vitro.

• Journal of Chest Surgery
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• v.30 no.6
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• pp.566-572
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• 1997

A major obstacles to evaluation of newly-developed treatment strategy for human lung cancer has been the lack of appropriate experimental animal models. We describe a new experimental model of orthotopically-developed non-small cell lung cancer in nude rat, involving inoculation of tumor cell suspension by thoracotomy. Over 40 direct implantation to the periphery of the lung has been performed to date, each requiring less than'1 hour for completion. This model has been used to perform a series of experiments to investigate whether the rat lung and surrounding structures trapped tumor cells with 2 different non-small cell lung cancer cell lines(NCI-H46O and NCI-H1299). Every animal showed development of tumor masses, which were loculated at the periphery of the lung karenchyma and identified also by radiography. After 3 weetu of the inoculation, tumor develop meat at the mediastinal strutures were identified. The life expectancies of the victims were different between the cell lines, but were approximately 5 weeks when NCI-H46O cell line was used. This new orthotopic lung cancer model may be facilitate future studies of the new therapeutics of localized non-small cell lung cancer .

• Bulletin of the Korean Chemical Society
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• v.31 no.9
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• pp.2649-2655
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• 2010

$PKC{\delta}$-catalytic V5 Heptapeptide (FEQFLDI, FP7) interacts with heat shock protein 27 (HSP27) and inhibits HSP27-mediated resistance to cell death against various stimuli including radiation therapy. Here, we prepared radio-iodinated heptapeptide and further investigated its uptake properties in HSP27 expression cells. Peptide sequence of FP7 and a negative control peptide (WSLLEKR, QP7) was modified by substituting their C-terminus residue to tyrosine (FP6Y and QP6Y) to label radio-iodine. Iodinated peptides were confirmed by LC mass analysis with cold iodine reaction mixture. Accumulation of [$^{125}I$]iodo-FP6Y and [$^{125}I$]iodo-QP6Y in NCI-H1299 cell line, with higher level of HSP27, and NCI-H460 cell line, with lower level of HSP27, was measured by NaI(Tl) scintillation counter. The modification of substituting C-terminus residue of FP7 to tyrosine (FP6Y) did not affect its interaction with HSP27. Accumulation of [$^{125}I$]iodo-FP6Y in NCI-H1299 cells was 3 fold higher than in NCI-H460 cells. The novel radio-iodinated FP6Y would be used as a tracer for targeting HSP27 protein.

• Journal of Environmental Science International
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• v.27 no.12
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• pp.1299-1303
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• 2018

This study was conducted to evaluate the growth performance of broilers fed different levels of Hermetia illucens powder. A total of 400 broiler chicks (1-day old Arbor Acres) were fed commercial diets containing H. illucens powder at 0%, 0.1%, 0.5%, and 1% with four replicates (25 chicks per replicate), for 35 days. Weight gain in broilers fed diets containing different levels of H. illucens powder increased significantly at 28 and 35 days, compared with that of the control (p<0.05). However, feed intake and mortality showed no differences among the treatments as a function of time. At 21, 28, and 35 days, broilers fed different levels of H. illucens powder had lower feed conversion rates (p<0.05) than their counterparts fed the control diet. In conclusion, 0.5% H. illucens powder is the optimal level for improved weight gain and feed conversion.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.7
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• pp.3223-3228
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• 2012

HMGN5 is a typical member of the HMGN (high mobility group nucleosome-binding protein) family which may function as a nucleosomal binding and transcriptional activating protein. Overexpression of HMGN5 has been observed in several human tumors but its role in tumorigenesis has not been fully clarified. To investigate its significance for human lung cancer progression, we successfully constructed a shRNA expression lentiviral vector in which sense and antisense sequences targeting the human HMGN5 were linked with a 9-nucleotide loop. Inhibitory effects of siRNA on endogenous HMGN5 gene expression and protein synthesis were demonstrated via real-time RT-PCR and western blotting. We found HMGN5 silencing to significantly inhibit A549 and H1299 cell proliferation assessed by MTT, BrdU incorporation and colony formation assays. Furthermore, flow cytometry analysis showed that specific knockdown of HMGN5 slowed down the cell cycle at the G0/G1 phase and decreased the populations of A549 and H1299 cells at the S and G2/M phases. Taken together, these results suggest that HMGN5 is directly involved in regulation cell proliferation in A549 and H1299 cells by influencing signaling pathways involved in cell cycle progression. Thus, our finding suggests that targeting HMGN5 may be an effective strategy for human lung cancer treatment.