Yoo, Hyuntae

Permanent URI for this collectionhttps://hdl.handle.net/10735.1/3730

Hyuntae Yoo is an Assistant Professor in the Department of Molecular and Cell Biology. He is also one of the Principal Investigators a the Center for Systems Biology. Dr Yoo's research seeks to discover "functional integration of genomic, proteomic and metabolomic studies to experimental models of human disease for discovery of novel drug targets." Learn more about Professor Yoo on his Faculty and Research and Research Explorer pages.

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Recent Submissions

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    The Distinct Metabolic Phenotype of Lung Squamous Cell Carcinoma Defines Selective Vulnerability to Glycolytic Inhibition
    (Springer Nature, 2018-08-20) Goodwin, Justin; Neugent, Michael L.; Lee, Shin Yup; Choe, Joshua H.; Choi, Hyunsung; Jenkins, Dana M. R.; Ruthenborg, Robin J.; Robinson, Maddox W.; Jeong, Ji Yun; Wake, Masaki; Abe, Hajime; Takeda, Norihiko; Endo, Hiroko; Inoue, Masahiro; Xuan, Zhenyu; Yoo, Hyuntae; Chen, Min; Ahn, Jung-Mo; Xuan, Zhenyu; Yoo, Hyuntae; Chen, Min; Ahn, Jung-Mo; Minna, John D.; Helke, Kristi L.; Singh, Pankaj K.; Shackelford, David B.; Kim, Jung-whan; Goodwin, Justin; Neugent, Michael L.; Lee, Shin Yup; Choe, Joshua H.; Choi, Hyunsung; Jenkins, Dana M. R.; Ruthenborg, Robin J.; Robinson, Maddox W.; Xuan, Zhenyu; Yoo, Hyuntae; Kim, Jung-whan
    Adenocarcinoma (ADC) and squamous cell carcinoma (SqCC) are the two predominant subtypes of non-small cell lung cancer (NSCLC) and are distinct in their histological, molecular and clinical presentation. However, metabolic signatures specific to individual NSCLC subtypes remain unknown. Here, we perform an integrative analysis of human NSCLC tumour samples, patient-derived xenografts, murine model of NSCLC, NSCLC cell lines and The Cancer Genome Atlas (TCGA) and reveal a markedly elevated expression of the GLUT1 glucose transporter in lung SqCC, which augments glucose uptake and glycolytic flux. We show that a critical reliance on glycolysis renders lung SqCC vulnerable to glycolytic inhibition, while lung ADC exhibits significant glucose independence. Clinically, elevated GLUT1-mediated glycolysis in lung SqCC strongly correlates with high F-18-FDG uptake and poor prognosis. This previously undescribed metabolic heterogeneity of NSCLC subtypes implicates significant potential for the development of diagnostic, prognostic and targeted therapeutic strategies for lung SqCC, a cancer for which existing therapeutic options are clinically insufficient.
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    Quantitative liver-specific protein fingerprint in blood: A signature for hepatotoxicity
    (2014-01-14) Hu, Z.; Lausted, C.; Yoo, Hyuntae; Yan, X.; Brightman, A.; Chen, J.; Wang, W.; Bu, X.; Hood, L.
    We discuss here a new approach to detecting hepatotoxicity by employing concentration changes of liver-specific blood proteins during disease progression. These proteins are capable of assessing the behaviors of their cognate liver biological networks for toxicity or disease perturbations. Blood biomarkers are highly desirable diagnostics as blood is easily accessible and baths virtually all organs. Fifteen liver-specific blood proteins were identified as markers of acetaminophen (APAP)-induced hepatotoxicity using three proteomic technologies: label-free antibody microarrays, quantitative immunoblotting, and targeted iTRAQ mass spectrometry. Liver-specific blood proteins produced a toxicity signature of eleven elevated and four attenuated blood protein levels. These blood protein perturbations begin to provide a systems view of key mechanistic features of APAP-induced liver injury relating to glutathione and S-adenosyl-L-methionine (SAMe) depletion, mitochondrial dysfunction, and liver responses to the stress. Two markers, elevated membrane- bound catechol-O-methyltransferase (MB-COMT) and attenuated retinol binding protein 4 (RBP4), report hepatic injury significantly earlier than the current gold standard liver biomarker, alanine transaminase (ALT). These biomarkers were perturbed prior to onset of irreversible liver injury. Ideal markers should be applicable for both rodent model studies and human clinical trials. Five of these mouse liver-specific blood markers had human orthologs that were also found to be responsive to human hepatotoxicity. This panel of liver-specific proteins has the potential to effectively identify the early toxicity onset, the nature and extent of liver injury and report on some of the APAP-perturbed liver networks.

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