Sun-Young Seo
Yonsei University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Sun-Young Seo's research lab focuses on cancer stem cell biology, particularly in glioblastoma and salivary gland disorders, with an emphasis on molecular mechanisms driving tumorigenesis, therapy resistance, and tissue regeneration. The lab investigates key transcription factors such as SOX2, OCT4, and NANOG in cellular reprogramming and malignant transformation, as well as signaling pathways like Notch and TGF-β in tumor progression. Using integrative 'omics' approaches—transcriptomics, ChIP-seq, and proteomics—the lab aims to identify novel therapeutic targets and develop effective treatments for aggressive cancers, especially through targeting glioblastoma stem cells and modulating the tumor microenvironment. The lab also explores regenerative and anti-inflammatory strategies in salivary gland diseases using animal models and organoids.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Jagged1 (JAG1) is a Notch ligand that contact-dependently activates Notch receptors and regulates cancer progression. The JAG1 intracellular domain (JICD1) is generated from JAG1, like formation of the NOTCH1 intracellular domain (NICD1); however, the role of JICD1 in tumorigenicity has not been comprehensively elucidated. Here we show that JICD1 induces astrocytes to acquire several cancer stem cell properties, including tumor formation, invasiveness, stemness, and resistance to anticancer ther
Introduction Salivary gland dysfunction, often resulting from salivary gland obstruction-induced inflammation, is a prevalent condition. Corticosteroid, known for its anti-inflammatory and immunomodulatory properties, is commonly prescribed in clinics. This study investigates the therapeutic implications and potential side effects of dexamethasone on obstructive sialadenitis recovery using duct ligation mice and salivary gland organoid models. Methods Functional and pathological changes were ass
Glioblastoma multiforme (GBM) is one of the most aggressive and lethal human brain tumors, and the median survival of patients with GBM is only 14 months. Glioblastoma stem cells (GSCs) are regarded as a main cause of GBM recurrence, because of their self-renewal and drug resistance properties. Therefore, targeting GSCs is an important therapeutic strategy for GBM. In this study, we show the effects of BRM270, a compound from natural plant extracts, on GSCs in vitro and GBM recurrence in vivo. B
Embryonic stem cell factors-OCT4, NANOG, and SOX2-contribute to the maintenance of stem cell properties and malignant progression in various cancers, including glioblastoma. Although functional roles of each of these genes are well documented in stem cell and cancer biology, no study has directly compared their cellular transforming activity under same experimental conditions. In this study, we compared the cellular transforming activity of OCT4, NANOG, and SOX2 using human immortalized astrocyt
Although lifespan-extended canine and porcine cells via SV40LT exhibit no apparent transforming changes, they are inappropriate for use as nuclei donors for SCNT because of their aneuploidy.
Glioblastoma (GBM) is the most aggressive and malignant brain tumor, resulting in a poor prognosis. The current therapy for GBM consists in concurrent radiation and chemotherapy following removal of the tumor. Although the therapy prolongs patient survival, recurrence often occurs. The major cause of tumor recurrence is thought to be GBM stem cells (GSCs), which aid the development of chemo-radiotherapy resistance, and can self-renew and aberrantly differentiate. Therefore, GSCs should be target
Glioblastoma (GBM) is the most lethal brain cancer, causing inevitable deaths of patients owing to frequent relapses of cancer stem cells (CSCs). The significance of the NOTCH signaling pathway in CSCs has been well recognized; however, there is no NOTCH-selective treatment applicable to patients with GBM. We recently reported that Jagged1 (JAG1), a NOTCH ligand, drives a NOTCH receptor-independent signaling pathway via JAG1 intracellular domain (JICD1) as a crucial signal that renders CSC prope
To elucidate the complex interplay of undifferentiated cancer cells in malignancy, we focus on the crucial mechanisms that maintain the undifferentiated state of cancer stem-like cells, which drive tumor growth and therapy resistance. Here, we identify a protein called dehydrogenase/reductase 13 (DHRS13) that is abundant in undifferentiated glioblastoma cells. DHRS13 is primarily located in the mitochondria and functions as a retinaldehyde reductase, converting all-trans-retinaldehyde to all-tra
Cancer stem-like cells (CSCs) are considered promising targets for anti-cancer therapy owing to their role in tumor progression. Extensive research is, therefore, being carried out on CSCs to identify potential targets for anti-cancer therapy. However, this requires the availability of patient-derived CSCs ex vivo, which remains restricted due to the low availability and diversity of CSCs. To address this limitation, a functional polymer thin-film (PTF) platform was invented to induce the transf
Notch ligands [jagged (JAG) and, delta-like (DLL) families] and receptors [NOTCH family] are key regulators of Notch signaling. NOTCH signaling contributes to vascular development, tissue homeostasis, angiogenesis, and cancer progression. To elucidate the universal functions of the JAG, DLL, and NOTCH families and their connections with various biological functions, we examined 15 types of cancer using The Cancer Genome Atlas clinical database. We selected the differentially expressed genes (DEG
Abstract Jagged1 (JAG1) is a Notch ligand that contact-dependently activates Notch receptors and regulates cancer progression. The JAG1 intracellular domain (JICD1) is generated from JAG1, such as the formation of NOTCH1 intracellular domain (NICD1), however, the role of JICD1 in tumorigenicity has not been comprehensively elucidated. Herein, we revealed that JICD1 induced astrocytes to acquire several cancer stem cell properties, including tumor formation, invasiveness, stemness, and resistance
Salivary gland (SG) stem cell-derived extracellular vesicles (EVs) are promising agents for regenerative therapy, but efficient production and targeted delivery remain key challenges. We developed a WNT3A-releasing double-layered microwell scaffold by integrating WNT3A-loaded poly(D,L-lactide-co-glycolide) (PLGA) nanofibers with a polycaprolactone (PCL)-based microwell array. This 3D platform promotes salivary gland epithelial stem cell (sgEpSC) spheroid formation and sustained biochemical stimu