Jungyeon Lee
Hanyang University · Biochemistry, Genetics and Molecular Biology
About the Lab
Professor Jungyeon Lee's research lab focuses on the molecular and epigenetic mechanisms underlying cancer progression, particularly in breast cancer. The lab investigates the roles of epigenetic regulators—such as DOT1L, NSD3, and RBP2—in tumor initiation, metastasis, and therapy resistance, with an emphasis on how these enzymes modulate histone modifications to influence gene expression programs driving epithelial-mesenchymal transition and cancer stem cell properties. The lab integrates molecular biology, genomics, and in vivo models to uncover novel therapeutic targets in hormone-resistant and aggressive cancers.
Research Overview
Research Output Trend
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Selected Papers
15This is one of the first empirical studies of the relationship between a developing country's system of intellectual property protection and the volume and composition of U.S. foreign direct investment in that country. Based on data obtained from almost one hundred U.S. firms regarding their perceptions of how weak or strong such protection is in various countries, the authors' results are consistent with the view that a country's system of intellectual property protection influences the volume
DOT1L has emerged as an anticancer target for MLL-associated leukaemias; however, its functional role in solid tumours is largely unknown. Here we identify that DOT1L cooperates with c-Myc and p300 acetyltransferase to epigenetically activate epithelial-mesenchymal transition (EMT) regulators in breast cancer progression. DOT1L recognizes SNAIL, ZEB1 and ZEB2 promoters via interacting with the c-Myc-p300 complex and facilitates lysine-79 methylation and acetylation towards histone H3, leading to
In a longitudinal quasi-field setting, we develop and test a compensatory process model of social network closure over time on the development of a transactive memory system (TMS) in groups. Although a great deal of research examines the effects of closure on organizational outcomes, that research does not describe the microprocesses that explain when, and under what conditions, closure is beneficial or detrimental. Results from our analysis of the microprocesses associated with TMSs revealed a
Earlier research on whistle-blowing in organizations has usually investigated whistle-blowing about wrongdoing of various types, with the possibility that results are influenced by the great variety of types of wrongdoing reported by whistle-blowers. Earlier research on sexual harassment has focused primarily on antecedents of the event and outcomes for the individual only, rather than organizational consequences. In this study we attempted to examine both questions: is sexual harassment differe
Abstract Histone methyltransferase NSD3 is frequently dysregulated in human cancers, yet the epigenetic role of NSD3 during cancer development remains elusive. Here we report that NSD3-induced methylation of H3K36 is crucial for breast tumor initiation and metastasis. In patients with breast cancer, elevated expression of NSD3 was associated with recurrence, distant metastasis, and poor survival. In vivo, NSD3 promoted malignant transformation of mammary epithelial cells, a function comparable t
Background: Despite the benefit of endocrine therapy, acquired resistance during or after treatment still remains a major challenge in estrogen receptor (ER)-positive breast cancer. We investigated the potential role of histone demethylase retinoblastoma-binding protein 2 (RBP2) in endocrine therapy resistance of breast cancer. Methods: Survival of breast cancer patients according to RBP2 expression was analyzed in three different breast cancer cohorts including METABRIC (n = 1980) and KM plotte
Polycomb protein chromobox homolog 7 (CBX7) is involved in several biologic processes including stem cell regulation and cancer development, but its roles in breast cancer remain unknown. Here, we demonstrate that CBX7 negatively regulates breast tumor initiation. CD44(+)/CD24(-)/ESA(+) breast stem-like cells showed diminished CBX7 expression. Furthermore, small hairpin RNA-mediated CBX7 knockdown in breast epithelial and cancer cells increased the CD44(+)/CD24(-)/ESA(+) cell population and rein
Research Areas
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