Jong Wan Park
Seoul National University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Jong Wan Park's research lab focuses on molecular mechanisms underlying cancer progression, with a central emphasis on hypoxia-inducible factors (HIFs), tumor microenvironment signaling, and epigenetic regulation. The lab investigates how transcription factors like HIF-1α and HIF-2α interact with oncogenic pathways such as Wnt/β-catenin, and explores the role of oxygen-sensing enzymes like PHDs and FIH in epigenetic control of metastasis. Additionally, the lab examines natural compounds—such as curcumin, EGCG, and chaetocin—as potential chemopreventive and therapeutic agents targeting HIF signaling and oxidative stress. The overarching goal is to identify novel molecular targets for cancer therapy, particularly in hepatoma and other aggressive malignancies.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Dot1-like protein (DOT1L) is an evolutionarily conserved histone methyltransferase that methylates lysine 79 of histone H3 (H3K79). Mammalian DOT1L participates in the regulation of transcription, development, erythropoiesis, differentiation, and proliferation of normal cells. However, the role of DOT1L in cancer cell proliferation has not been fully elucidated. DOT1L siRNA-transfected A549 or NCI-H1299 lung cancer cells displayed a nonproliferating multinucleated phenotype. DOT1L-deficient cell
RATIONALE: Nasal polyposis implies a refractory clinical course in case of chronic rhinosinusitis (CRS). Although hypoxia is believed to be associated with nasal polyposis, little is known about the mechanism underlying polypogenesis. OBJECTIVES: To determine if hypoxia drives nasal polyposis by epithelial-to-mesenchymal transition (EMT). METHODS: Immunoblotting, immunofluorescence, flow cytometry, and real-time polymerase chain reaction were performed to evaluate EMT and hypoxic markers in huma
Harmful effects of high fructose intake on health have been widely reported. Although fructose is known to promote cancer, little is known about the underlying mechanisms. Here, we found that fructose triggers breast cancer metastasis through the ketohexokinase-A signaling pathway. Molecular experiments showed that ketohexokinase-A, rather than ketohexokinase-C, is necessary and sufficient for fructose-induced cell invasion. Ketohexokinase-A-overexpressing breast cancer was found to be highly me