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임혜원,홍선택,진욱,임승환,김수정,강현정,박은희,안기섭,임창진 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.5
Reactive oxygen species (ROS) are involved in a diversity of important phenomena in the process of tumor development. To investigate the alterations of oxidative stress and their related systems in tumor progression, a variety of components in the antioxi-dative stress defense system were examined in prostate cancer cell lines, PC3 and LNCaP. Cell surface molecules involved in metastasis were expressed highly in PC3 cells compared with LNCaP cells, and strong invasion ability was shown in PC3 cells only. ROS level in LNCaP cells was twice higher than that in PC3 cells, although nitric oxide (NO) level was similar between the two cell lines. The content of GSH increased up to about 2-fold in PC3 compared with LNCaP. Activities of glutathione reductase, thioredoxin reductase, and glutathione S-trans-ferase except catalase are significantly higher in PC3 cells than in LNCaP cells. Furthermore, oxidative stress-inducing agents caused down-regulation of GSH and glutathione S-transferase much more significantly in LNCaP cells than in PC3 cells. These results imply that malignant tumor cells may main-tain low ROS content by preserving relatively high anti-oxidative capacity, even in the presence of stressful agents.
TGF-β 신호 전달계에 의한 염증 제어를 통한 암 억제 효과
김윤재,홍선택 대한암예방학회 2009 Journal of cancer prevention Vol.14 No.4
Transforming growth factor-β (TGF-β) has a dual role in tumorigenesis as a tumor suppressor or a tumor promoter. In normal cells, TGF-β suppresses the initiation of cell transformation by inhibiting cell growth and inducing cell apoptosis. However, TGF-β also modulates processes such as motility, invasion, immune surveillance and angiogenesis of tumorigenic cells in their late stage or metastatic stage. These paradoxical characteristics may depend on contextual, developmental and tissue-specific conditions. Cross-talk between tumor cells and their surrounding microenvironment is crucial during tumorigenesis. In particular, inflammatory microenvironment can induce cells to undergo transformations by supplying inflammatory cytokines and inhibiting immune system. Because TGF-βhas been known to suppress immune system, it is important to understand the regulation of inflammatory signaling by TGF-β during tumorigenesis. Our group has published that TGF-β signaling mediators such as Smad6 and Smad7 inhibit inflammatory processes by blocking the recruitment of adaptors to cognate receptors and mediating the anti-inflammatory function of TGF-β. Based on the previous data, it will be useful to find new therapeutic reagents that can specifically induce Smad proteins or inhibit inflammatory signaling through highthroughput screening of natural products or chemical library.
Inflammasome as a Therapeutic Target for Cancer Prevention and Treatment
HaThiHuyenTrang,홍선택 대한암예방학회 2017 Journal of cancer prevention Vol.22 No.2
Chronic inflammation is a critical modulator of carcinogenesis through secretion of inflammatory cytokines, which leads to the formation of an inflammatory microenvironment. In this process, the inflammasome plays an important role in the expression and activation of interleukin (IL)-1 and IL-18 to promote cancer development. The inflammasome is a multiprotein complex consisting of several nucleotide-binding domain and leucine-rich repeat containing receptor, adaptor proteins, and caspase 1 (CASP1). It senses the various intracellular (damage-associated molecular patterns) and extracellular (pathogen-associated molecular patterns) stimuli. A primed inflammasome recruits adaptor proteins, activates CASP1 to enhance the proteolytic cleavage of pro-IL-1β and IL-18, and sends the signal to respond to each insult. Depending on stimuli and cell contexts, several inflammasomes are closely associated with the initiation and promotion of carcinogenesis. In contrast, inflammasomes also show an ambivalent effect on carcinogenesis by enhancing inflammatory cell death (pyroptosis) and repairing damaged tissues. Although the inflammasome plays a controversial role in carcinogenesis, it may be a promising target for human cancer prevention and treatment. A more in-depth study on the role of the inflammasome in carcinogenesis, based on stimuli, cell contexts, and cancer stages, can lead to the development of novel therapeutic strategies against malignant human cancers.
이현승,김세현,김지훈,배은진,홍선택,박이병,김유진,이시훈 대한내분비학회 2011 Endocrinology and metabolism Vol.26 No.2
Neurofibromatosis type 1 (NF1) is one of the most common autosomal dominant inherited disorders affecting the nervous system. NF1 is associated with mutations in the NF1 gene, which is located on chromosome sub-band 17q11.2 and contains 57 exons spanning approximately 300 kb of genomic DNA. NF1 is caused by a loss of function mutation of the NF1 gene, a tumor suppressor gene, which encodes for neurofibromin, a GTPase-activating protein (GAP) involved in the negative regulation of Ras activity. The GAP-related domain, which is encoded for by exons 20-27a, is one of the most important functional domains in neurofibromin. The cysteine-serine-rich domain has been recognized as an important functional domain in NF1-related pheochromocytomas. As the result of many genetic analyses of NF1-related pheochromocytomas, pheochromocytoma has generally been recognized as a true component of NF1. We recently experienced two families with NF1 accompanied by pheochromocytoma. The proband of family 1 is a 31-year-old female diagnosed with NF1 and pheochromocytoma. Gene analysis of the proband and her sister showed that the mutation of the NF1 gene (c.7907+1G>A) led to the skipping of exon 53 during NF1 mRNA splicing. The proband of family 2 is a 48-year-old male who was diagnosed with the same condition. Gene analysis demonstrated the mutation of the NF1 gene (c.5206-8C>G) with missplicing of exon 37. These novel germline mutations did not fall into the GAP-related nor the cysteine-serine-rich domains, but into the C-terminal area of the NF1 gene. This suggests that the correlation between the genotype and phenotype of NF1-related pheochromocytoma is somewhat difficult to characterize. Further studies will be necessary to confirm the function of the C-terminal area of the NF1 gene and its contribution to the development of NF1 and pheochromocytoma.
전기자동차 충전 인터페이스를 통한 차량 진단 서비스를 제공하는 CAN-to-Ethernet 게이트웨이 설계
이은조(Eunjo Lee),김석명(Seok-Myung Kim),김선경(Seon-Kyung Kim),엄광식(Kwang-Sik Eom),홍선택(Sun-Taek Hong) 한국자동차공학회 2017 한국자동차공학회 학술대회 및 전시회 Vol.2017 No.11
The most widely installed Ethernet recently applies to vehicle diagnostics, drivers can easily access electric control units (ECUs) using in-vehicle network (IVN) Ethernet to controller area network (CAN) gateway to check and reprogram the latest firmware from remote sites. The parallel ECU programming through Ethernet is a new remarkable on-board diagnostic (OBD) service which can provide programming for multiple ECUs at the same time. However, the service provokes the ECU programming completion time delay because of the burst frames and bus arbitrations. This paper presents a time-scheduling architecture for the gateway minimizes the delay of ECU programming completion time at the same time which can be applied to the electric vehicle charging controller using the power line communication (PLC) interface.
대장암 세포주 HT29에서 NS-398 처리시 유전자 발현 양상의 cDNA Microarray 분석
서현주 ( Seo Hyeon Ju ),김영호 ( Kim Yeong Ho ),손희정 ( Son Hui Jeong ),이풍렬 ( Lee Pung Lyeol ),김재준 ( Kim Jae Jun ),이종철 ( Lee Jong Cheol ),김대식 ( Kim Dae Sig ),정지원 ( Jeong Ji Won ),홍선택 ( Hong Seon Taeg ) 대한소화기학회 2003 대한소화기학회 추계학술대회 Vol.2003 No.-
기존의 여러 연구 연구에서 NSAIDs의 대장암에 대한 항종양효과가 보고되었지만 이의 작용기전은 아직도 밝혀지지 않고 있다. 현재까지 NSAIDs의 항종양효과와 관련한 대표적인 분자표적은 cyclooxygenase-2 (COX-2) 효소인데 COX-2의 억제에 따른 prostaglandin 생성 저해를 통해 대장암세포의 apoptosis 유발, 세포분열과 신생혈관생성의 억제, 세포부착분자의 변조에서 기인하는 전이의 억제 등을 통해 항종양효과를 나타낸다고