Jo Sung-yoon
Korea University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Jo Sung-yoon's research lab focuses on the molecular mechanisms underlying metabolic regulation, aging-related diseases, and cancer progression, with a particular emphasis on oncometabolites, RNA epigenetics, and tumor microenvironment remodeling. The lab investigates how metabolic shifts—driven by factors such as mTORC1 signaling, m6A RNA modification, and aging-associated metabolites like methylmalonic acid—affect cellular homeostasis and disease pathogenesis. Key research directions include the role of signaling pathways (e.g., SPHK1/HIF-1α, AKT/GSK-3β) in cancer under hypoxia, the regulation of lipid and glucose metabolism via natural compounds (e.g., linalool, lemon balm essential oil), and the crosstalk between adipose tissue, liver, and fibroblasts in metabolic and neoplastic disorders. The lab integrates molecular biology, metabolomics, and systems biology approaches to uncover novel therapeutic targets in metabolic and oncological diseases.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15The antioxidant activity of lemon balm (Melissa officinalis) essential oil (LBEO) on 2,2-diphenyl-1-picrylhydrazyl (DPPH) radicals and its hypoglycaemic effect in db/db mice were investigated. LBEO scavenged 97 % of DPPH radicals at a 270-fold dilution. Mice administered LBEO (0.015 mg/d) for 6 weeks showed significantly reduced blood glucose (65 %; P < 0.05) and TAG concentrations, improved glucose tolerance, as assessed by an oral glucose tolerance test, and significantly higher serum insulin
Sphingosine kinase 1 (SPHK1) is a newly discovered modulator of hypoxia inducible factor 1α (HIF-1α) with various biological activities such as cell growth, survival, invasion, angiogenesis, and carcinogenesis. Thus, in the present study, the biological mechanisms of melatonin were elucidated in association with SPHK1 pathway in PC-3 prostate cancer cells under hypoxia. Melatonin inhibited the stability of HIF-1α in a time- and concentration- dependent manners. Also, melatonin decreased SPHK1 ac
Significance N6-methyladenosine (m 6 A) is the most prevalent modification in eukaryotic messenger RNA (mRNA) and affects RNA metabolism including splicing, stability, and translation. The m 6 A methyltransferase complex (MTC) is responsible for generating the m 6 A modifications in mRNA; however, the regulation of m 6 A modification is still unclear. We have identified Mechanistic Target of Rapamycin Complex 1 (mTORC1) as a key regulator of MTC and demonstrate that mTORC1 can stabilize MTC via
Adipose tissue lipolysis produces glycerol and nonesterified fatty acids (NEFA) that serve as energy sources during nutrient scarcity. Adipose tissue lipolysis is tightly regulated and excessive lipolysis causes hepatic steatosis, as NEFA released from adipose tissue constitutes a major source of TG in the liver of patients with nonalcoholic fatty liver diseases. Here we show that the liver-enriched transcription factor CREBH is activated by TG accumulation and induces FGF21, which suppresses ad
The systemic metabolic shifts that occur during aging and the local metabolic alterations of a tumor, its stroma and their communication cooperate to establish a unique tumor microenvironment (TME) fostering cancer progression. Here, we show that methylmalonic acid (MMA), an aging-increased oncometabolite also produced by aggressive cancer cells, activates fibroblasts in the TME, which reciprocally secrete IL-6 loaded extracellular vesicles (EVs) that drive cancer progression, drug resistance an
We investigated hypocholesterolemic mechanisms of linalool, an aromatic anti-oxidative monoterpene, which is abundant in teas and essential oils. Oral administration of linalool to mice for 6 weeks significantly lowered total and low-density lipoprotein cholesterol concentrations, and HMG-CoA reductase protein expression (-46%; P<0.05) by both transcriptional and posttranscriptional mechanisms. Linalool suppressed the gene expression of HMG-CoA reductase by reducing the binding of SREBP-2 to its
Serine/one-carbon metabolism provides critical resources for nucleotide biosynthesis and epigenetic maintenance and is thus necessary in cancer cell growth, although the detailed regulatory mechanisms remain unclear. We uncover a critical role of glycogen synthase kinase 3 (GSK3) in regulating the expression of serine/one-carbon metabolic enzymes. Nuclear enrichment of GSK3 significantly suppresses genes that mediate de novo serine synthesis, including PHGDH, PSAT1, PSPH, and one-carbon metaboli
The mechanistic target of rapamycin (mTOR) pathway senses and integrates various environmental and intracellular cues to regulate cell growth and proliferation. As a key conductor of the balance between anabolic and catabolic processes, mTOR complex 1 (mTORC1) orchestrates the symphonic regulation of glycolysis, nucleic acid and lipid metabolism, protein translation and degradation, and gene expression. Dysregulation of the mTOR pathway is linked to numerous human diseases, including cancer, neu
Diet influences macronutrient availability to cells, and although mechanisms of sensing dietary glucose and amino acids are well characterized, less is known about sensing lipids. We defined a nutrient signaling mechanism involving fatty acid-binding protein 5 (FABP5) and mechanistic target of rapamycin complex 1 (mTORC1) that is activated by the essential polyunsaturated fatty acid (PUFA) ω-6 linoleic acid (LA). FABP5 directly bound to the regulatory-associated protein of mTOR (Raptor) to enhan
Abstract Background Ectodomain shedding of GPIbα, a proteolytic event in which metalloprotease ADAM17 cleaves the Gly464-Val465 bond and releases glycocalicin to the plasma, is considered a critical step in mediating clearance of stored platelets. Supporting evidence has been obtained from animal studies using ADAM17 inhibitors. However, the definitive proof is lacking due to the broad substrate specificity of ADAM17. We report herein novel monoclonal antibodies (MAbs) that specifically inhibit