• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.769-773
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• 2014

Fangchinoline (Fan) inhibits cell proliferation and induces apoptosis in several cancer cell lines. The effects of Fan on cell growth and proliferation in breast cancer cells remain to be elucidated. Here, we show that Fan inhibited cell proliferation in the MDA-MB-231 breast cancer cell line through suppression of the AKT/Gsk-3beta/cyclin D1 signaling pathway. Furthermore, Fan induced apoptosis by increasing the expression of Bax (relative to Bcl-2), active caspase 3 and cytochrome-c. Fan significantly inhibited cell proliferation of MDA-MB-231 cells in a concentration and time dependent manner as determined by MTT assay. Flow cytometry analysis demonstrated that Fan treatment of MDA-MB-231 cells resulted in cell cycle arrest at the G1 phase, which correlated with apparent downregulation of both mRNA and protein levels of both PCNA and cyclin D1. Further analysis demonstrated that Fan decreased the phosphorylation of AKT and GSK-3beta. In addition, Fan up-regulated active caspase3, cytochrome-c protein levels and the ratio of Bax/Bcl-2, accompanied by apoptosis. Taken together, these results suggest that Fan is a potential natural product for the treatment of breast cancer.

• The Journal of Information Systems
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• v.27 no.1
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• pp.171-191
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• 2018

Purpose Corporate technology leakage is not only monetary loss, but also has a negative impact on the corporate image and further deteriorates sustainable growth. In particular, since SMEs are highly dependent on core technologies compared to large corporations, loss of technology leakage threatens corporate survival. Therefore, it is important for SMEs to "prevent and protect technology leakage". With the recent development of data analysis technology and the opening of public data, it has become possible to discover and proactively detect companies with a high probability of technology leakage based on actual company data. In this study, we try to construct profiles of enterprises with and without technology leakage experience through profiling analysis using data mining techniques. Furthermore, based on this, we propose a classification model that distinguishes companies that are likely to leak technology. Design/methodology/approach This study tries to develop the empirical model for prevention and protection of technology leakage through profiling method which analyzes each SME from the viewpoint of individual. Based on the previous research, we tried to classify many characteristics of SMEs into six categories and to identify the factors influencing the technology leakage of SMEs from the enterprise point of view. Specifically, we divided the 29 SME characteristics into the following six categories: 'firm characteristics', 'organizational characteristics', 'technical characteristics', 'relational characteristics', 'financial characteristics', and 'enterprise core competencies'. Each characteristic was extracted from the questionnaire data of 'Survey of Small and Medium Enterprises Technology' carried out annually by the Government of the Republic of Korea. Since the number of SMEs with experience of technology leakage in questionnaire data was significantly smaller than the other, we made a 1: 1 correspondence with each sample through mixed sampling. We conducted profiling of companies with and without technology leakage experience using decision-tree technique for research data, and derived meaningful variables that can distinguish the two. Then, empirical model for prevention and protection of technology leakage was developed through discriminant analysis and logistic regression analysis. Findings Profiling analysis shows that technology novelty, enterprise technology group, number of intellectual property registrations, product life cycle, technology development infrastructure level(absence of dedicated organization), enterprise core competency(design) and enterprise core competency(process design) help us find SME's technology leakage. We developed the two empirical model for prevention and protection of technology leakage in SMEs using discriminant analysis and logistic regression analysis, and each hit ratio is 65%(discriminant analysis) and 67%(logistic regression analysis).

• Maxillofacial Plastic and Reconstructive Surgery
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• v.35 no.3
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• pp.143-154
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• 2013

Purpose: This study was to find efficacy of integrin alpha2 (${\alpha}_2$) and epidermal growth factor receptor (EGFR) as tumor marker of oral squamous cell carcinoma (SCC) and clarify the selective cell death effect of anti-integrin ${\alpha}_2$ and anti-EGFR on SCC cells, additionally testify conjugated gold nanoparticles (GNP) with air plasma for selective cell death of oral SCC. Methods: Expression of integrin ${\alpha}_2$, EGFR on human SCC cells (SCC25) were examined by western blot. SCC25 cells were treated with anti-integrin ${\alpha}_2$, anti-EGFR and analysed by Hemacolor staining, immunoflorescence staining, FACS flow cytometry. Conjugated GNP with integrin ${\alpha}_2$, EGFR antibody were treated by air plasma on SCC cells. Results: Integrin ${\alpha}_2$ and EGFR were over-expressed on SCC25 cells than normal lung WI-38 cells. The cell viability rate of SCC25 cells treated with anti-integrin ${\alpha}_2$, anti-EGFR was lower than WI-38 cells. The concentration changes of nucleus, releasing cytochrome c and apoptosis inducing factor (AIF) from mitochondria to cytosol were observed. The changes of proteins related with apoptosis were observed. Increase of bax, bcl-xL, activation of caspase-3, -7, -9, and fragmentation of PARP, DFF45 and decrease of lamin A/C in SCC25 cells were observed. In FACS, increase of sub-$G_1$ and S phase was observed. Cell cycle related proteins, Such as cyclin D1, cyclin dependent kinase (CDK) 4, cyclin A, cyclin E, CDK 2, p27 were decreased. After SCC25 cells treated with conjugatged GNP-Integrin ${\alpha}_2$, GNP-EGFR, additionally air plasma, the cell death rate was significantly increased. Conclusion: Integrin ${\alpha}_2$, EGFR were over-expressed in oral SCC cells. Anti-integrin ${\alpha}_2$, anti-EGFR in SCC25 cells induced apoptosis selectively. When GNP-anti integrin ${\alpha}_2$, GNP-anti EGFR were treated with air plasma on SCC25 cells, cancer cells were died more selectively. GNP-anti integrin ${\alpha}_2$, GNP-anti EGFR with air plasma could be treatment choice of oral SCC.

• Journal of Distribution Science
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• v.12 no.12
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• pp.83-92
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• 2014

Purpose - A business ecosystem refers to mutually dependent systems interconnected by a loose foundation of various ecosystem members such as customers, suppliers, partners, and other stakeholders. The ecosystem-based strategy attempts to achieve competitive advantage for firms by enriching a business ecosystem or building a sustainable business ecosystem through the collaboration and co-evolution of its members. A sustainable business ecosystem is a source of competitiveness for firms anda manageable resource for gaining a competitive advantage. Customers represent the core membership of the business ecosystem and play a pivotal role in building a sustainable business ecosystem. This study examines the effects of customer participation on economic and social value in the business ecosystem and suggests a course of action for building a sustainable business ecosystem. Research design, data, and methodology - Two business cases of South Korea are selected from two different business types: business-to-business (B2B) and business-to-customer (B2C) firms. Business ecosystems for B2B and B2C firms reflect contrasting characteristics. Data was collected from in-depth interviews with four representatives of four firms. Results - The study suggested seven propositions for the relationships between customer participation and a sustainable business ecosystem through multiple case studies based on in-depth interviews. The results reveal the following four strategic actions for building sustainable business ecosystems based on the suggested propositions: alignment, systemization, socialization, and co-evolution. Alignment refers to achieving a harmonic balance or virtuous circle among the firm's mission, investment, and value creation. Systemization refers to building and implementing management and infrastructure systems rooted in the corporate culture. Socialization of customers in the business ecosystem reinforces the harmony or virtuous cycle. Finally, co-evolution is associated with the relationship between firms and customers as buyer firms in a restricted business ecosystem. Conclusions - This study considers multiple cases for the execution of a sustainable business ecosystem in collaboration with customers and suggests seven propositions and four strategic actions. The results are based on qualitative data from interviews with business associates from two firms in an open business ecosystem and two firms in a restricted business ecosystem, both in South Korea. Our research results regarding two contrasting business ecosystems shed light on business issues and policy making in Asian business environments, which are in the transition stages from a traditional conglomerate-driven to an inclusive growth-driven economy. The business ecosystem itself should be considered a manageable resource for firms' competitive positions in the market. A customer is a member of the business ecosystem and should thus be viewed not only as a purchasing entity and an object of relationship management but also as a co-creator of value. Therefore, firms should collaborate with customers to build sustainable business ecosystems. For this, firms must create social value, which cannot be created by customers alone, within the business ecosystem. Then, customers participate in a business ecosystem and build it to be favorable to them. Implications for academics and practitioners were suggested.

• Reproductive and Developmental Biology
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• v.35 no.2
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• pp.151-157
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• 2011

Clinical arthritis is typically divided into rheumatoid arthritis (RA) and osteoarthritis (OA). Arthritis-induced muscle weakness is a major problem in aged people, leading to a disturbance of balance during the gait cycle and frequent falls. The purposes of the present study were to confirm fiber type-dependent expression of muscle atrophy markers induced by arthritis and to identify the relationship between clinical signs and expression of muscle atrophy markers. Mice were divided into four experimental groups as follows: (1) negative control (normal), (2) positive control (CFA+acetic acid), (3) RA group (CFA+acetic acid+type II collagen), and (4) aging-induced OA group. DBQA/1J mice (8 weeks of age) were injected with collagen (50 ${\mu}g/kg$), and physiological (body weight) and pathological (arthritis score and paw thickness) parameters were measured once per week. The gastrocnemius muscle from animals in each group was removed, and the expression of muscle atrophy markers (MAFbx and MuRF1) and myosin heavy chain isoforms were analyzed by reverse transcription-polymerase chain reaction. No significant change in body weight occurred between control groups and collagen-induced RA mice at week 10. However, bovine type II collagen induced a dramatic increase in clinical score or paw thickness at week 10 (p<0.01). Concomitantly, the expression of the muscle atrophy marker MAFbx was upregulated in the RA and OA groups (p<0.01). A dramatic reduction in myosin heavy chain (MHC)-$I{\beta}$ was seen in the gastrocnemius muscles from RA and OA mice, while only a slight decrease in MHC-IIb was seen. These results suggest that muscle atrophy gene expression occurred in a fiber type-specific manner in both RA- and OA-induced mice. The present study suggests evidence regarding why different therapeutic interventions are required between RA and OA.

• Journal of Life Science
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• v.17 no.4 s.84
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• pp.522-528
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• 2007

In the present investigation, we studied the modulating effects of caffeic acid, chlorogenic acid, and (-)-epigallocatechin-3-gallate(EGCG) on the methylation status of promoter regions of cell cycle regulator, p16, in human breast cancer T-47D cells. We demonstrated that treatment of T-47D cells with caffeic acid, chlorogenic acid, or EGCG partially inhibited the methylation status of the promoter regions of p16 genes determined by methylation-specific PCR. In contrast, unmethylated p16 genes were increased with the treatment of T-47D cells with $20{\mu}M$ of caffeic acid or chlorogenic acid for 6 days. Treatment of T-47D cells with 5, 20 or $50{\mu}M$ of EGCG increased the unmethylation status of p16 gene up to 100%, and the methylation-specific bands of this gene were decreased up to 50% in a concentration-dependent manner. The finding of present study demonstrated that coffee polyphenols and EGCG have strong inhibitory effects of the cellular DNA methylation process through increased formation of S-adenosyl-homocysteine(SAH) during the catechol-O-methyltransferase (COMT)- mediated O-methylation of these dietary chemicals or an direct inhibition of the DNA methyltransferases. In conclusion, various dietary polyphenols could reverse the methylation status of p16 gene in human breast T-47D cells.

• Journal of Life Science
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• v.18 no.6
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• pp.884-890
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• 2008

Genistein, an isoflavone in soybean products, is a potential chemopreventive agent against various types of cancer. There are several studies documenting molecular alterations leading to cell cycle arrest at G2/M phase and induction of apoptosis; however, its mechanism of action and its molecular targets on the prostaglandin $E_2$ ($PGE_2$) production and telomere length regulation in human cancer remain unclear. In this study, we investigated the effect of genistein on the levels of cyclooxygenases (COXs) and telomere regulatory components of several human cancer cell lines (T24, human bladder carcinoma cells; U937, human leukemic cells; AGS, human stomach adenocarcinoma cells and SK-MEL-2, human skin melanoma cells). Genistein treatment resulted in the inhibition of cancer cell proliferation in a concentration-dependent manner. It was found that genistein treatment markedly decreased the levels of COX-2 mRNA and protein expression without significant changes in the expression of COX-1, which was correlated with a decrease in $PGE_2$ synthesis. Genistein treatment also partly inhibited the levels of human telomerase reverse transcriptase (hTERT) as well as human telomerase RNA (hTR) and telomerase-associated protein (TEP)-1, and the activity of telomerase. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of genistein.

• Biomolecules & Therapeutics
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• v.20 no.6
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• pp.538-543
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• 2012

The Maillard Reaction Products (MRPs) are chemical compounds which have been known to be effective in chemoprevention. Death receptors (DR) play a central role in directing apoptosis in several cancer cells. In our previous study, we demonstrated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal, a MRP product, inhibited human colon cancer cell growth by inducing apoptosis via nuclear factor-${\kappa}B$ (NF-${\kappa}B$) inactivation and $G_2$/M phase cell cycle arrest. In this study, (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate, a new (E)-2,4-bis(p-hydroxyphenyl)-2-butenal derivative, was synthesized to improve their solubility and stability in water and then evaluated against NCI-H460 and A549 human lung cancer cells. (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate reduced the viability in both cell lines in a time and dose-dependent manner. We also found that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate increased apoptotic cell death through the upregulation of the expression of death receptor (DR)-3 and DR6 in both lung cancer cell lines. In addition to this, the transfection of DR3 siRNA diminished the growth inhibitory and apoptosis inducing effect of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate on lung cancer cells, however these effects of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate was not changed by DR6 siRNA. These results indicated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate inhibits human lung cancer cell growth via increasing apoptotic cell death by upregulation of the expression of DR3.

• Journal of Life Science
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• v.27 no.2
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• pp.164-171
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• 2017

Our previous study suggested that S-allylcysteine (SAC) inhibits the proliferation of the human cervical cancer cell line, HeLa, at least in part through the induction of apoptosis and cell cycle arrest. To further analyze the specific molecular mechanism(s) by which SAC mediates its antiproliferative effects, this study examined the role of SAC in regulating the protein expression of initiator caspase (caspase-9), effector caspases (caspase-3 and caspase-7), and poly-ADP-ribose polymerase (PARP) in HeLa. Western blot analysis showed that when cells were treated with 50 mM SAC for 48 hr, the expression of procaspase-3, -7, and -9 and PARP was reduced by 94%, 38%, 95%, and 64%, respectively, as compared to the untreated control. In contrast, the expression of caspase-3, -7, and -9 and cleaved-PARP was markedly increased by SAC treatment. The SAC-mediated changes in the expression of these proteins were correlated with the concomitant inhibition of cellular proliferation by SAC. The cell proliferation assay showed that HeLa treatment with more than 20 mM SAC for 6-48 hr resulted in both concentration- and time-dependent inhibition of cellular proliferation. These results indicate that the SAC-induced antiproliferative effect in HeLa may be mediated at least in part through the activation of caspase-9, followed by the activation of caspase-3 and caspase-7 as well as the inactivation of PARP, thus leading to cellular apoptosis.

• KDI Journal of Economic Policy
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• v.35 no.2
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• pp.71-105
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• 2013

Now that fiscal soundness is increasingly important influenced by the euro area fiscal crisis, early budget execution has been under the spotlight as a tool for economy control, other than typical expansionary method, such as supplementary budget. Basically, early budget execution is a fiscal policy instrument that reponses to economic fluctuations through modifying the inter-temporal allocation of fiscal expenditure within budget, without affecting fiscal soundness. This study empirically examines how effective the intert-temporal reallocation of fiscal expenditure is in economy control. Using Korea's Consolidated Fiscal data, the size of inter-temporal reallocation of fiscal expenditure is defined as changes of fiscal expenditure for one year excluding seasonal factors and used to explain real economic growth rate, a dependent variable. The result shows that the macroeconomic effect of the inter-temporal reallocation turns out meaningful in general, though some policy time lag exists. Meanwhile, a simulation using macroeconomic model finds that overall effect on economic growth is not large because increase in fiscal expenditure allocation at a certain point of time is canceled by the opposite direction within the same fiscal year. However, the inter-temporal reallocation is found to reduce volatility of key macroeconomic variables so as to contribute to partially stabilizing macroeconomy. In particular, such effect of economic stabilization seems to be highly apparent at the time of financial crisis, but not very noticeable in normal economic cycle.