Seoyeon Lee
Yonsei University · Medicine
About the Lab
Professor Seoyeon Lee's research lab focuses on the molecular and metabolic mechanisms underlying cancer progression, particularly the interplay between cellular metabolism, epithelial-mesenchymal transition (EMT), and tumor metastasis. The lab investigates how oncogenic signaling pathways such as Wnt and TGF-β reprogram cancer cell metabolism—shifting toward glycolysis and glutaminolysis—to support tumor growth, invasion, and stemness. A central theme is the role of the tumor microenvironment, including hypoxia and necrotic cell-derived signals like HMGB1, in promoting aggressive cancer phenotypes. The lab also explores how metabolic reprogramming intersects with DNA damage responses and redox signaling (e.g., ROS) in radiotherapy resistance and metastasis.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Radiation therapy is one of the major tools of cancer treatment, and is widely used for a variety of malignant tumours. Radiotherapy causes DNA damage directly by ionization or indirectly via the generation of reactive oxygen species (ROS), thereby destroying cancer cells. However, ionizing radiation (IR) paradoxically promotes metastasis and invasion of cancer cells by inducing the epithelial-mesenchymal transition (EMT). Metastasis is a major obstacle to successful cancer therapy, and is close
Rapidly growing malignant tumors frequently encounter hypoxia and nutrient (e.g., glucose) deprivation, which occurs because of insufficient blood supply. This results in necrotic cell death in the core region of solid tumors. Necrotic cells release their cellular cytoplasmic contents into the extracellular space, such as high mobility group box 1 (HMGB1), which is a nonhistone nuclear protein, but acts as a proinflammatory and tumor-promoting cytokine when released by necrotic cells. These rele
Wnt signaling plays a critical role in embryonic development, and its deregulation is closely linked to the occurrence of a number of malignant tumors, including breast and colon cancer. The pathway also induces Snail-dependent epithelial-to-mesenchymal transition (EMT), which is responsible for tumor invasion and metastasis. In this study, we show that Wnt suppresses mitochondrial respiration and cytochrome C oxidase (COX) activity by inhibiting the expression of 3 COX subunits, namely, COXVIc,
Most cancer cells depend on enhanced glucose and glutamine (Gln) metabolism for growth and survival. Oncogenic metabolism provides biosynthetic precursors for nucleotides, lipids, and amino acids; however, its specific roles in tumor progression are largely unknown. We previously showed that distal-less homeobox-2 (Dlx-2), a homeodomain transcription factor involved in embryonic and tumor development, induces glycolytic switch and epithelial-mesenchymal transition (EMT) by inducing Snail express
Metastasis is a major obstacle to the efficient and successful treatment of cancer. Initiation of metastasis requires epithelial‐mesenchymal transition (EMT) that is regulated by several transcription factors, including Snail and ZEB1/2. EMT is closely linked to the acquisition of cancer stem cell (CSC) properties and chemoresistance, which contribute to tumor malignancy. Tumor suppressor p53 inhibits EMT and metastasis by negatively regulating several EMT‐inducing transcription factors and regu
BACKGROUND: The results of recent studies suggest that factors in rural environments may protect against the development of allergic diseases, but the underlying mechanisms are not well understood. The aim of this study was to investigate the prevalence of allergic diseases, to establish if this prevalence is influenced by migration from rural to urban areas and to identify environmental risk factors associated with these diseases. METHODS: A cross-sectional study of children aged 9-12 years fro
The crack formation mechanism of O3-type Na<sub>0.8</sub>Mg<sub>0.2</sub>Fe<sub>0.4</sub>Mn<sub>0.4</sub>O<sub>2</sub> due to air-exposure is directly evidenced using <italic>in situ</italic> mass spectrometry and various atomic-scale analyses.
Epithelial-mesenchymal transition (EMT) and oncogenic metabolism (including glycolytic switch) are important for tumor development and progression. Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced by TGF-β and Wnt and regulates TGF-β- and Wnt-induced EMT and glycolytic switch by activating Snail. We also found that TGF-β/Wnt suppressed cytochrome c oxidase (COX), the terminal enzyme of the mit
BACKGROUND: In contrast to tumor-suppressive apoptosis and autophagic cell death, necrosis promotes tumor progression by releasing the pro-inflammatory and tumor-promoting cytokine high mobility group box 1 (HMGB1), and its presence in tumor patients is associated with poor prognosis. Thus, necrosis has important clinical implications in tumor development; however, its molecular mechanism remains poorly understood. RESULTS: In the present study, we show that Distal-less 2 (Dlx-2), a homeobox gen
Lymphatic malformations are fluid-filled congenital defects of lymphatic channels occurring in 1 in 6000 to 16,000 patients. There are various types, and they often exist in conjunction with other congenital anomalies and vascular malformations. Great strides have been made in understanding these malformations in recent years. This review summarize known molecular and embryological precursors for lymphangiogenesis. Gene mutations and dysregulations implicated in pathogenesis of lymphatic malform
Treatment with bronchodilators such as LAMA or LABA was effective in improving lung function in patients with bronchiectasis, regardless of concurrent treatments that also improve lung function. These data may support the use of LAMA and LABA in patients with bronchiectasis.
The industrial manufacturing process for Ni-rich layered oxides for Li-ion batteries includes a washing step to remove residual Li compounds, such as LiOH and Li 2 CO 3, from the oxide surface. However, Ni-rich layered oxides are deformed during a conventional water-based washing process, leading to the degradation of the oxide surface. In this regard, a significant challenge for Ni-rich layered oxides is to remove residual Li compounds without surface damage during a washing process. Herein, th
Research Areas
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