Education
B.S. (with High Honors), University of California at Davis
M.S., University of Rochester, School of Medicine and Dentistry
Ph.D., University of Rochester, School of Medicine and Dentistry
Post-doctoral training, Sungkyunkwan University, School of Medicine (Suwon, Korea)
Background
Kyung U. Hong received his B.S. degree in Environmental Toxicology from UC Davis (Davis, CA) and his M.S. and Ph.D. degrees in Toxicology from the University of Rochester, School of Medicine and Dentistry (Rochester, NY). Before joining Western New England University in 2023, he was an Assistant Professor at the Department of Pharmacology and Toxicology at the University of Louisville, School of Medicine (Louisville, KY).
One of his passions is teaching. At WNE, he teaches basic and advanced pharmacology courses, as well as cardiovascular pathophysiology and drugs at the College of Pharmacy and Health Sciences. Throughout his career in academics, he has trained numerous high school, undergraduate, graduate, and professional students.
Dr. Hong is also an avid researcher. He has more than 25 years of experience in biomedical research. The main area of his expertise is in so-called Pharmacogenomics (and Toxicogenomics). His current research focuses on understanding how genetic factors (e.g., N-acetyltransferase 2 gene) interact with environmental factors (e.g., dietary consumption of heterocyclic amines in cooked meat) and how the interaction modifies the risk of developing metabolic disorders, such as hyperlipidemia and insulin resistance. As of February 2024, Dr. Hong has contributed 45 peer-reviewed research articles.
Research Interests
- Pharmacogenomics of N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2)
- Metabolic effects of dietary consumption of heterocyclic amines via cooked meat
- Link between genetic polymorphism in NAT2 and risk of hyperlipidemia.
- Regulation of polyamine homeostasis by NAT1 and NAT2.
- Role of cytoskeleton-associated protein 2 (CKAP2) and cytoskeleton-associated protein 2-like (CKAP2L) in mitosis and during mammalian brain development.
Arylamine N-acetyltransferases (NAT1 and NAT2) are traditionally known as phase II metabolic enzymes that often detoxify and eliminate certain foreign substances, including drugs and toxicants. Individuals carry different variants of NAT1 and NAT2 genes (we call this, ‘genetic polymorphism.’), which determine their capacity to metabolize certain foreign substances. In plain language, some individuals are susceptible to the toxic effects of drugs or toxicants due to their genetic makeup (e.g., depending on the variants of the NAT1/2 gene they carry). One of Dr. Hong’s research projects involves a class of dietary toxicants, called heterocyclic amines (HCAs). HCAs are produced when cooking meat at high temperatures or for a long period of time. “Unhealthy” cooking methods, such as frying, broiling, and grilling, favor the formation of these compounds. He recently reported that dietary consumption of HCAs can induce metabolic dysfunction in the liver and potentially contribute to the development of insulin resistance (a pre-diabetic state), hyperglycemia (high blood sugar), type II diabetes, and fatty liver disease [1]. Moreover, his research findings suggest that certain individuals (i.e., rapid acetylators) are genetically susceptible to the toxic effects of HCAs.
In addition, Dr. Hong has been working on another novel area of research. It is to understand why individuals that exhibit a higher activity of NAT2 (i.e., rapid acetylators) are at a greater risk of developing hyperlipidemia [2]. Hyperlipidemia (high fat or cholesterol level in the blood) increases one’s risk of developing atherosclerosis and cardiometabolic disorders. Thus, it is important to identify and investigate genetic and environmental factors that contribute to the development of this pathological condition. He is currently trying to tackle this interesting problem by using liver cancer cells that are genetically engineered to express varying levels of NAT2.
Another project he is working on is unrelated to the others. Years ago, he and his colleagues first described the molecular functions of a novel cancer-associated protein, called cytoskeleton associated protein 2 (CKAP2). CKAP2 regulates the dynamics of the spindle microtubules during mitosis (cell division). Depletion of CKAP2 in cells undergoing mitosis results in defects in chromosome segregation and genomic instability. Recently, he observed that CKAP2 is robustly expressed in the developing mouse brain, especially in the cell layer that harbors neural stem/progenitor cells. Growth and differentiation of neural progenitor cells contribute to brain size and functions. What is CKAP2 doing in neural progenitor cells? Is CKAP2 required for proper growth and maturation of the mammalian brain? To answer these questions, he plans to knockout (delete) the mouse Ckap2 gene specifically in the developing brain and study the consequences of not having CKAP2 during brain development.
Scholarly Works
Select Peer-Reviewed Articles: (Last 5 years)
For a complete list of publications, go to: https://www.ncbi.nlm.nih.gov/myncbi/kyung.hong.2/bibliography/public/
(*, Student co-author)
*Walls KM, Hong KU, Hein DW. 2023. Induction of glucose production by heterocyclic amines is dependent on N-acetyltransferase 2 genetic polymorphism in cryopreserved human hepatocytes. Toxicol Lett. 383:192-195. PMID: 37423373.
Hong KU, Hein DW. 2023. N-acetyltransferase 2 haplotype modifies risks for both dyslipidemia and urinary bladder cancer. Pharmacogenet Genomics. 33(6):136-137. PMID: 37306342
Hong KU, *Walls KM, Hein DW. 2023. Non-coding and intergenic genetic variants of human arylamine N-acetyltransferase 2 (NAT2) gene are associated with differential plasma lipid and cholesterol levels and cardiometabolic disorders. Front Pharmacol. 14:1091976. PMID: 37077812.
*Walls KM, Hong KU, Hein DW. 2023. Heterocyclic amines reduce insulin-induced AKT phosphorylation and induce gluconeogenic gene expression in human hepatocytes. Arch Toxicol. 97(6):1613-1626. PMID: 37005939.
Hong KU, *Tagnedji AF, Doll MA, *Walls KM, Hein DW. 2023. Upregulation of cytidine deaminase in NAT1 knockout breast cancer cells. J Cancer Res Clin Oncol. 149(8):5047-5060. PMID: 36329350.
Hong KU, *Gardner JQ, Doll MA, Stepp MW, Wilkey DW, Benz FW, Cai J, Merchant ML, Hein DW. 2022. Dataset for proteomic analysis of arylamine N-acetyltransferase 1 knockout MDA-MB-231 breast cancer cells. Data Brief. 45:108634. PMID: 36426076.
Hong KU, Gardner JQ, Doll MA, Stepp MW, Wilkey DW, Benz FW, Cai J, Merchant ML, Hein DW. 2022. Proteomic analysis of arylamine N-acetyltransferase 1 knockout breast cancer cells: Implications in immune evasion and mitochondrial biogenesis. Toxicol Rep. 9:1566-1573. doi: 10.1016/j.toxrep.2022.07.010. PMID: 36158865.
Hong KU, Salazar-González RA, *Walls KM, Hein DW. 2022. Transcriptional Regulation of Human Arylamine N-Acetyltransferase 2 Gene by Glucose and Insulin in Liver Cancer Cell Lines. Toxicol Sci. 190(2):158-172. doi: 10.1093/toxsci/kfac103. PMID: 36156098.
Doll MA, *Ray AR, Salazar-González RA, Shah PP, Vega AA, Sears SM, Krueger AM, Hong KU, Beverly LJ, Hein DW. 2022. Deletion of arylamine N-acetyltransferase 1 in MDA-MB-231 human breast cancer cells reduces primary and secondary tumor growth in vivo with no significant effects on metastasis. Mol Carcinog. 61(5):481-493. doi: 10.1002/mc.23392. PMID: 35133049
Hong KU, Doll MA, Lykoudi A, Salazar-González RA, Habil MR, *Walls KM, Bakr AF, Ghare SS, Barve SS, Arteel GE, Hein DW. 2020. Acetylator Genotype-Dependent Dyslipidemia in Rats Congenic for N-Acetyltransferase 2. Toxicol Rep. 7:1319-1330. doi: 10.1016/j.toxrep.2020.09.011. PMID: 33083237.
Carlisle SM, Trainor PJ, Hong KU, Doll MA, Hein DW. 2020. CRISPR/Cas9 knockout of human arylamine N-acetyltransferase 1 in MDA-MB-231 breast cancer cells suggests a role in cellular metabolism. Sci Rep. 10(1):9804. PMID: 32555504.
Stepp MW, Salazar-González RA, Hong KU, Doll MA & Hein DW. 2019. N-acetyltransferase 1 Knockout Elevates Acetyl Coenzyme A Levels and Reduces Anchorage-independent Growth in Human Breast Cancer Cell Lines. J Oncol. 2019:3860426. PMID: 31531019.
