Yongbaek Kim
Seoul National University · 医学
研究室紹介
Professor Yongbaek Kim's research lab focuses on the molecular mechanisms underlying cancer progression, with a particular emphasis on tumor microenvironment interactions, metabolic reprogramming, and epigenetic regulation in cancer. The lab investigates how hypoxia, cancer-associated fibroblasts, and altered lipid metabolism contribute to tumor heterogeneity, drug resistance, and cancer stemness. Using advanced 'omics' technologies such as RNA-seq, MeDIP-seq, and next-generation sequencing, the lab explores signaling pathways and non-coding RNAs—including microRNAs—in various cancers, especially malignant mesothelioma and liver neoplasms. The ultimate goal is to identify novel therapeutic targets and understand drug resistance mechanisms, including those involving metformin and mitochondrial dysfunction.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15BACKGROUND: Hypoxia is a hallmark of the solid tumor microenvironment and is associated with poor outcomes in cancer patients. The present study was performed to investigate mechanisms underlying the hypoxia-induced phenotypic changes using human malignant mesothelioma (HMM) cells. METHODS: Hypoxic conditions were achieved by incubating HMM cells in the air chamber. The effect of hypoxia on phenotype changes in HMM cells was investigated by performing in vitro clonogenicity, drug resistance, mig
The role of microRNAs (miRNAs) as a post-transcriptional gene regulator has been elucidated in a broad range of organisms including domestic animals. Characterization of miRNAs in normal tissues is an important step to investigate the functions of miRNAs in various physiological and pathological conditions. Using Illumina Next Generation Sequencing (NGS) technology, we identified a total of 292 known and 329 novel miRNAs in normal horse tissues including skeletal muscle, colon and liver. Distinc
The molecular pathogenesis of chemically induced hepatocellular neoplasms and hepatoblastomas in the B6C3FI mouse is unclear but may involve alterations in the fi-catenin/Wnt signaling pathway as was recently described for human liver neoplasms. The objectives of this research were to characterize the mutation frequency and spectrum of P-catenin mutations and the intracellular localization of I-catenin protein accumulation in chemically induced hepatoblastomas and hepatocellular neoplasms. In th
BACKGROUND: Cancer-associated fibroblasts (CAFs) coordinate the malignancy of cancer cells via secretory materials. Reprogrammed lipid metabolism and signaling play critical roles in cancer biology. Oleic acid (OA) serves as a source of energy under glucose-deficient conditions, but its function in cancer progression remains unclear. The present study investigated that CAFs in xenografted tumors had higher amounts of fatty acids, particularly OA, compared to normal fibroblasts, and promoted the
Intratumoral heterogeneity is a hallmark of all cancers and functions as the major barrier against effective cancer therapy. In contrast to genetic mutations, the role of epigenetic modifications in the generation and maintenance of heterogeneous cancer cells remains largely undetermined. This study was performed to evaluate the epigenetic mechanisms involved in the tumor cell heterogeneity using side population (SP) and non-SP cells isolated from a human malignant mesothelioma (HMM) cell line.
Metformin, a drug for type 2 diabetes mellitus, has shown therapeutic effects for various cancers. However, it had no beneficial effects on the survival rate of human malignant mesothelioma (HMM) patients. The present study was performed to elucidate the underlying mechanism of metformin resistance in HMM cells. Glucose-starved HMM cells had enhanced resistance to metformin, demonstrated by decreased apoptosis and autophagy and increased cell survival. These cells showed abnormalities in mitocho
Studies were performed to determine the effects of Bcell suppression on the pathogenesis of Subgroup J avian leukosis virus (ALV-J) in broiler chickens. Neonatal chickens were treated with cyclophosphamide (CY) or PBS, and then infected with ALV-J (ADOL-7501) at 2 weeks of age. CY treatment induced B cell specific immunosuppression throughout the experiment confirmed by decreased bursal weight, intact lymphocyte mitogenetic activity stimulated by Con A and increased relative subpopulation of CD3
Glycated hemoglobin A1c (HbA1c) is widely used for monitoring and diagnosing human diabetes mellitus, but is rarely used in veterinary clinics. The goal of our study was to validate the commercial HbA1c testing system SD A1cCare analyzer (Bionote, Gyeoggi-do, South Korea) for use in dogs. Dogs were recruited with owner’s consent. Diabetic status was determined based on clinical signs, fasting hyperglycemia, and glycosuria. Intra-assay precision and linearity were evaluated with EDTA, heparin, or
Cyclophosphamide (CY) is an immunosuppressant and inhibits cell division by alkylating nucleic acids. This study was performed to determine the toxic effects of CY treatment in broiler chickens. One-d-old White Plymouth Rock broiler chickens were treated with either 4 mg/d CY or phosphate buffered saline (PBS) for 4 consecutive days. Mortality of the CY-treated chickens was 65.4% (34/52), while that of the PBS-treated chickens was 10% (5/50). CY-treated chickens were significantly smaller and ha
Infection with avian leukosis virus subgroup J (ALV-J) causes severe economic losses in the broiler industry by increasing mortality, producing tumors, and decreasing weight gain in chickens. The quantitation of ALV-J is difficult because of its failure to produce a cytopathic effect in cell culture systems and the nonspecificity of antigen-capture enzyme-linked immunosorbent assay (ELISA) tests. This study was performed to develop a quantitative competitive-reverse transcriptase-polymerase chai
A 4-mo-old male Japanese white-naped crane (Grus vipio) kept in an outdoor exhibit at the Everland Zoological Gardens in Korea became depressed and developed anorexia, weight loss, and diarrhea. Death of this bird was associated with an overwhelming systemic infection by an intracellular coccidian parasite, which resulted in necrosis and granulomatous inflammation in a number of major organs, including the intestine, liver, spleen, and kidney. Coccidian parasite-laden macrophages were commonly f