Kyounghyun Kim
Assistant Professor
Also affiliated: University of North Carolina at Chapel Hill (2024); Texas Tech University (2009); University of Seoul (2008); Texas A&M Health Science Center (2009–2025); Ministry of Agriculture and Forestry (2007); The University of Texas MD Anderson Cancer Center (2010); Taiwan Livestock Research Institute (2007); Seoul National University (2022); Chungbuk National University (2006); Eli Lilly (United States) (2012); Texas A&M University System (2006–2008); Yonsei University (2004–2016); Korea University (1999–2023); Severance Hospital (2018–2022); HCA Healthcare (2009); Cincinnati Health Department (2019); Texas College (2003–2009); Mitchell Institute (2010–2011); Asan Medical Center (2011–2020); Cheonan Yonam College (2007); University of California San Diego (2007); The Institute of Medical Science, Asahi Life Foundation (2007); National Cancer Center (2010); Gene Therapy Laboratory (2007); Texas A&M Health Science Center (2011); National Cancer Center (2010–2023); University of Veterinary Medicine (2006); Pohang TechnoPark (South Korea) (1998); CHA University (2013); Korea University (1999); Czech Academy of Sciences, Institute of Physiology (2006); Hanyang University (2001); Ajou University (2011); University of Cincinnati (2011–2020); Lanzhou University (2009); Newcastle University (2007); The University of Texas Southwestern Medical Center (2019); Catholic Kwandong University (2001); Texas A&M University (1996–2025); University of Cincinnati Medical Center (2014–2021)
Faculty Researcher
COM | Pharmacology & Toxicology
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Kyounghyun Kim's research focuses on the molecular mechanisms underlying various diseases, with a particular emphasis on cancer. Dr. Kim investigates how specific transcription factors, such as Sp1, influence gene expression in the context of neoplastic growth. His work has explored the role of the androgen receptor in regulating GPER1 transcription in prostate cancer cells and how the loss of the orphan nuclear receptor NR2E3 impacts Wnt/β-catenin signaling in hepatocellular carcinoma through epigenetic modifications and interactions with Sp1 and p300.
Further research by Dr. Kim extends to the influence of endocrine-disrupting chemicals on pancreatic diseases and cancer, examining the activity of the aryl hydrocarbon receptor. His publications also address broader health topics, including the association between body composition and chronic rhinosinusitis, and the contribution of type 2 diabetes mellitus to cardiovascular outcomes in cancer survivors. Dr. Kim leads a research group at the University of Arkansas for Medical Sciences and has an h-index of 32 with over 6,300 citations across 132 publications.
Metrics
- h-index: 32
- Publications: 132
- Citations: 6,363
Selected Publications
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Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling (2026)
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Abstract 1276: Dual epigenetic-kinase targeting to overcome resistance and immune evasion in hepatocellular carcinoma. (2026)
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Abstract 440: Dual epigenetic targeting of hepatocellular carcinoma (2025)
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The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma (2024)
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The Role of Endocrine Disruption Chemical-Regulated Aryl Hydrocarbon Receptor Activity in the Pathogenesis of Pancreatic Diseases and Cancer (2024)
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Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma (2024)
Collaboration Network
Top Collaborators
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- Abstract 440: Dual epigenetic targeting of hepatocellular carcinoma
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
- Abstract 1276: Dual epigenetic-kinase targeting to overcome resistance and immune evasion in hepatocellular carcinoma.
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
- Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma
- Abstract 1276: Dual epigenetic-kinase targeting to overcome resistance and immune evasion in hepatocellular carcinoma.
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
- Dual Targeting of EZH2 and LSD1 Suppresses Hepatocellular Carcinoma via Disruption of Sonic Hedgehog Signaling
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