Education
BS (with High Honors), University of California at Davis
MS, University of Rochester, School of Medicine and Dentistry
PhD, University of Rochester, School of Medicine and Dentistry
Post-doctoral training, Sungkyunkwan University, School of Medicine (Suwon, Korea)
Background
Dr. Hong earned his BS degree in Environmental Toxicology from the University of California, Davis, and his MS and PhD degrees in Toxicology from the University of Rochester School of Medicine and Dentistry. Before joining Western New England University (WNE) in 2023, he served as an Assistant Professor in the Department of Pharmacology and Toxicology at the University of Louisville School of Medicine.
One of his passions is teaching. At WNE, Dr. Hong teaches both foundational and advanced pharmacology courses, as well as cardiovascular pathophysiology and pharmacotherapy in the College of Pharmacy and Health Sciences. A dedicated educator, he has mentored high school, undergraduate, graduate, and professional students throughout his career.
Dr. Hong is also an active researcher with more than 25 years of experience in biomedical sciences, particularly in the fields of pharmacogenomics and toxicogenomics. His current research investigates how genetic variation—such as polymorphisms in the N-acetyltransferase 2 (NAT2) gene—interacts with environmental exposures, including dietary intake of heterocyclic amines from cooked meats, to influence susceptibility to metabolic disorders such as hyperlipidemia and insulin resistance. As of Aug 2025, he has authored or co-authored 50 peer-reviewed publications.
Research Interests
- Pharmacogenomics of N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2), with a focus on genetic polymorphisms and their impact on drug and toxicant metabolism.
- Metabolic effects of dietary heterocyclic amines (HCAs) formed in cooked meats, particularly their role in insulin resistance, hyperglycemia, type 2 diabetes, and fatty liver disease.
- Genetic variation in NAT2 and risk of dyslipidemia, with emphasis on hyperlipidemia and cardiometabolic disorders.
- Regulation of polyamine homeostasis by NAT2, and implications for cell growth and metabolic regulation.
- Role of cytoskeleton-associated protein 2 (CKAP2) and CKAP2-like (CKAP2L) in mitotic spindle dynamics, chromosome segregation, genomic stability, and mammalian brain development.
1. NAT1/2 Genetic Polymorphisms and Dietary Toxicants (Heterocyclic Amines)
Arylamine N-acetyltransferases (NAT1 and NAT2) are phase II metabolic enzymes best known for detoxifying and eliminating foreign compounds, including many drugs and toxicants. Because individuals carry different genetic variants (polymorphisms) of NAT1 and NAT2, their ability to metabolize these compounds varies. In practical terms, genetic differences in NAT1/2 can make some people more vulnerable to the harmful effects of drugs or environmental toxicants.
One of Dr. Hong’s primary research interests is in heterocyclic amines (HCAs), a class of toxic compounds formed during high-temperature or prolonged meat cooking (e.g., frying, broiling, grilling). His laboratory recently reported that dietary exposure to HCAs can induce hepatic metabolic dysfunction and may contribute to the development of insulin resistance, hyperglycemia, type 2 diabetes, and fatty liver disease. Importantly, his findings indicate that individuals with the rapid NAT2 acetylator phenotype are genetically predisposed to heightened susceptibility to HCA-induced toxicity.
2. NAT2 and Risk of Dyslipidemia
Building on his work in pharmacogenomics, Dr. Hong is also investigating why individuals with higher NAT2 activity (rapid acetylators) appear to have a greater risk of developing dyslipidemia. Dyslipidemia, characterized by elevated blood levels of cholesterol and triglycerides, is a major risk factor for atherosclerosis and cardiometabolic disorders.
To address this novel question, Dr. Hong is employing genetically engineered liver cancer cell models that express different levels of NAT2. By manipulating NAT2 expression, his laboratory is working to determine the molecular mechanisms linking NAT2 activity to lipid metabolism and cardiovascular risk.
3. CKAP2 in Cancer and Brain Development
A distinct line of Dr. Hong’s research focuses on cytoskeleton associated protein 2 (CKAP2), a novel cancer-associated protein he and colleagues first characterized. CKAP2 regulates spindle microtubule dynamics during mitosis, and its depletion leads to errors in chromosome segregation and genomic instability—a hallmark of cancer.
More recently, Dr. Hong’s group discovered that CKAP2 is robustly expressed in the developing mouse brain, particularly in the neural progenitor cell layer. Since the growth and differentiation of neural progenitor cells determine brain size and function, this finding raises intriguing questions: What role does CKAP2 play in neural progenitor cell biology? Is CKAP2 essential for proper brain development? To address these questions, his team is developing a conditional knockout mouse model in which the Ckap2 gene is deleted specifically in the developing brain. This work will clarify CKAP2’s role in neural stem/progenitor cell dynamics and mammalian neurodevelopment.
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*, Joh JY*, Martinez MM, Hong KU, Hein DW. 2025. Metabolic effects of heterocyclic amines on insulin‑induced AKT phosphorylation and gluconeogenic gene expression are modified by N -acetyltransferase 2 genetic polymorphism. Pharmacogenet Genomics. 35(4):119-126. PMID: 39878101.
Hong KU, Aureliano AP*, Walls KM*, Hein DW. 2024. Investigation on regulation of N-acetyltransferase 2 expression by nuclear receptors in human hepatocytes. Front Pharmacol. 15:1488367. PMID: 39624836.
Kwon H*, Joh JY*, Hong KU. 2024. Human CKAP2L shows a cell cycle-dependent expression pattern and exhibits microtubule-stabilizing properties. FEBS Open Bio. 14(9):1526-1539. PMID: 39073037.
Walls KM*, Joh JY*, Hong KU, Hein DW. 2024. Heterocyclic Amines Disrupt Lipid Homeostasis in Cryopreserved Human Hepatocytes. Cardiovasc Toxicol. 24(8):747-756. doi: 10.1007/s12012-024-09874-1. PMID: 38851663.
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.
