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Dietary Phytochemical을 이용한 화학적 암에방과 그 작용 기전
서영준,이종민,Surh, Young-Joon,Lee, Jong-Min 한국환경성돌연변이발암원학회 1998 한국환경성돌연변이·발암원학회지 Vol.18 No.1
Chemoprevention refers to the use of non-toxic chemical agents to prevent the neoplastic development by inhibiting, delaying, or reversing a multi-stage carcinogenesis. The primary goal of chemoprevention research is to identify or produce effective agents and strategies for clinical trials for applications to normal or high risk human populations. A large number of compounds have been tested for their possible chemopreventive activities, and it is of interest to note that many of them are naturally occurring substances. Thus, a variety of plant and vegetable constituents, particularly those included in our daily diet, have been found to possess substantial protective properties against experimental carcinogenesis. These substances, collectively known as dietary phytochemicals, exert their chemopreventive effects by influencing specific step(s) of multi-stage carcinogenesis: some inhibit metabolic activation or enhance detoxification of carcinogens, others interfere with covalent interactions between ultimate eloctrophilic carcinogens and the target cell DNA and still others may exert anti-promoting or anti-progressing effects. Mechanism-based interventions by use of safe dietary phytochemicals may provide one of the most practical and promising cancer chemopreventive strategies.
Heme oxygenase-1 유도를 통한 화학 암예방 및 세포보호와 그 분자생물학적 기전
김은희,김성환,나혜경,서영준,Kim, Eun-Hee,Kim, Sung-Hwan,Na, Hye-Kyung,Surh, Young-Joon 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.4
Heme oxygenase(HO)-1 is an important antioxidant enzyme that plays a pivotal role in cellular adaptation and protection in response to a wide array of noxious stimuli. Thus, HO-1 induction has been associated with prevention or mitigation of pathogenesis of various diseases, including acute inflammation, atherosclerosis, degenerative diseases, and carcinogenesis. Recent progress in our understanding of the function of molecules in the cellular signaling network as key modulators of gene transcription sheds light on the molecular mechanisms underlyuing HO-1 gene expression. A panel of redox-sensitive transcription factors such as activator protein-1, nuclear factor-kB, and nuclear factor E2-related factor-2, and some of the upstream kinases have been identified as prime regulators of HO-1 gene induction. This review summarizes molecular mechanisms underlying HO-1 expression and the significance of targeted induction of HO-1 as a potential chemopreventive or chemoprotective strategy.
Tumor suppressor p16^(INK4a) in Cancer
이미현(Mee-Hyun Lee),최부영(Bu-Young Choi),서영준(Young-Joon Surh) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.3
p16^(INK4a) is a tumor suppressor that belongs to the INK4 family of the cyclin D-dependent kinases (cdk) inhibitors. It plays regulatory roles in cell proliferation and in tumorigenesis by interacting with Rb signaling. Abnormally elevated p16^(INK4a) protein expression causes cell cycle arrest (G1/S transition) and loss of cyclincdk activity. In many cancers, p16^(INK4a) is altered by mutation, deletion, and promoter methylation. This review summarizes the function of p16 as an important regulator of cancer pathobiology and a promising target for developing cancer therapeutic and chemopreventive agents.
김정환(Jung-Hwan Kim),나혜경(Hye-Kyung na),서영준(Young-Joon Surh) 한국환경성돌연변이발암원학회 2002 한국환경성돌연변이·발암원학회지 Vol.22 No.4
Dioxin represents a group of halogenated aromatic hydrocarbons of which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is well known for its extremely toxic properties as well as ubiquitous presence in our environment and ecosystems. In order to better assess the carcinogenic mechanism of dioxin, we should utilize the reliable biomarkers that can precisely and correctly reflect multi-stage carcinogenesis. When MCF10A cells were exposed to TCDD (10 nM), expression of both CYP1A1 and CYP1B1 was induced in a time-related<br/> manner. The expression as well as activity of ornithine decarboxylase was transiently induced by TCDD treatment. In contrast, the induction of COX-2 that is implicated in carcinogenesis as well as inflammation, was not induced by TCDD. In another study, gap-junctional intercellular communication (GJIC) was attenuated by TCDD treatment as revealed by the dye-transfer assay. Based on these findings, TCDD has both tumor initiating<br/> and promoting potential in human breast epithelial cells in culture. Also, treatment of MCF10A cells with the carcinogen 7,12-dimethylbenz[a]anthracene plus TCDD resulted in malignant cell transformation as revealed by increased anchorage-independent growth of exposed cells. Additional studies may be necessary to<br/> assess the effects of TCDD on multi-stage carcinogenesis in vivo.
새로운 Anthraquinone 유도체, DHAQ-97의 항암작용: 아폽토시스에 의한 인체 유방암세포 사멸 유도
허연진(Yeon-Jin Hurh),김정환(Jung-Hwan Kim),장정희(Jung-Hee Jang),안병준(Byung-Zun Ahn),서영준(Young-Joon Surh) 한국환경성돌연변이발암원학회 2000 한국환경성돌연변이·발암원학회지 Vol.20 No.1
DHAQ-97, (2-(3-[p-bis(2-chloroethyl)aminophenyl]-2-formylaminopropanoyloxy)methyl-1,4-dihydroxy-9,10-anthraquinone), is a novel anthraquinone derivative synthesized for use as an anti-neoplastic agent. In the present study, we have evaluated the selective cytotoxicity of DHAQ-97 by comparing its effects on viability and proliferation of human breast cancer cell line (MCF-7) versus normal immortalized breast epithelial cell line (MCF-10A). Thus, DHAQ-97 reduced both viability and proliferation of MCF-7 cells to a much greater extent than did for MCF-10A cells. The growth inhibitory and anti-proliferative properties of DHAQ-97 appear to be attributable to its ability to induce apoptosis as revealed by positive staining after in situ nick-end labeling<br/> (TUNEL), cleavage of poly(ADP-ribose)polymerase, release of mitochondrial cytochrome c into cytoplasm, and increased expression of pro-apoptotic Bax protein. Recent studies have indicated possible involvement of the ubiquitous eukaryotic transcription factor, NF-kappa B (NF-kB) in the regulation of apoptotic cell death. In line with this notion, the NF-kB inhibitor pyrrolidine dithiocarbamate significantly attenuated the DHAQ-97-induced cytotoxicity in cultured MCF-7 cells. Furthermore, mild activation of NF-kB, as determined by its increased DNA binding capability, was observed 30 min after treatment with 10 μM DHAQ-97. Taken together, the above findings suggest that DHAQ-97 exerts selective cytotoxicity towards cancer cells through induction of<br/> apoptosis, which appears to be regulated by NF-kB.