Kyungmin Lee
Hanyang University · 医学
研究室紹介
Professor Kyungmin Lee's research lab focuses on molecular mechanisms underlying cancer progression and therapeutic resistance, particularly in breast cancer subtypes such as triple-negative and estrogen receptor-positive breast cancers. The lab investigates key oncogenic drivers like MYC, PRR11, and ECM1, as well as signaling pathways involving NF-κB, STING, and PI3K, to uncover targets for immunotherapy and precision medicine. Additionally, the lab explores biomaterials for biomedical applications, including functionalized titanium coatings for orthopedic and dental implants through plasma electrolytic oxidation. These interdisciplinary efforts bridge cancer biology, immunology, and materials science to develop novel therapeutic strategies and advanced biomaterials.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Cyclooxygenase-2 (COX-2) is a major contributor to the elevation of spinal prostaglandin E2, which augments the processing of nociceptive stimuli following peripheral inflammation, and dynorphin has been shown to have an important role in acute and chronic pain states. Moreover, the transcription factor, nuclear factor-kappa B (NF-kB), regulates the expressions of both COX-2 and dynorphin. To elucidate the role of spinal NF-kB in the induction of inflammatory pain hypersensitivity, we examined w
INTRODUCTION: Extracellular matrix protein 1 (ECM1) is a secreted glycoprotein with putative functions in cell proliferation, angiogenesis and differentiation. Expression of ECM1 in several types of carcinoma suggests that it may promote tumor development. In this study, we investigated the role of ECM1 in oncogenic cell signaling in breast cancer, and potential mechanisms for its effects. METHODS: In order to find out the functional role of ECM1, we used the recombinant human ECM1 and viral tra
The MYC oncogene is frequently amplified in triple-negative breast cancer (TNBC). Here, we show that MYC suppression induces immune-related hallmark gene set expression and tumor-infiltrating T cells in MYC-hyperactivated TNBCs. Mechanistically, MYC repressed stimulator of interferon genes (STING) expression via direct binding to the STING1 enhancer region, resulting in downregulation of the T-cell chemokines CCL5, CXCL10, and CXCL11. In primary and metastatic TNBC cohorts, tumors with high MYC
Abstract The 17q23 amplicon is associated with poor outcome in ER + breast cancers, but the causal genes to endocrine resistance in this amplicon are unclear. Here, we interrogate transcriptome data from primary breast tumors and find that among genes in 17q23, PRR11 is a key gene associated with a poor response to therapeutic estrogen suppression. PRR11 promotes estrogen-independent proliferation and confers endocrine resistance in ER + breast cancers. Mechanistically, the proline-rich motif-me
Immune checkpoint blockades (ICBs) have revolutionized cancer treatment. Recent studies have revealed a subset of triple-negative breast cancer (TNBC) to be considered as an immunogenic breast cancer subtype. Characteristics of TNBC, such as higher mutation rates and number of tumor-infiltrating immune cells, render the immunogenic phenotypes. Consequently, TNBCs have shown durable responses to ICBs such as atezolizumab and pembrolizumab in clinic. However, a significant number of TNBC patients
The electrochemical characteristics of ZrO2 incorporated titanium oxide film on pure titanium were investigated via high energy plasma electrolytic oxidation (PEO) coating. To incorporate ZrO2 particles into the titanium oxide film, ZrO2 particles dispersed in the K3PO4 electrolyte were used in the study, which was compared to the result without ZrO2 particles. After the PEO process at a current density of 200 mA cm−2, most of the ZrO2 particles migrated toward the anodic titanium surface due to
Abstract Triple negative breast cancer is the most virulent subtype of this malignancy. Although initially responsive to cytotoxic chemotherapy, most patients with TNBC eventually develop drug-resistant disease. We previously reported co-amplification of MYC and MCL1 in a cohort of TNBCs after neoadjuvant chemotherapy (Balko et al. Cancer Discov. 2014). In addition, MYC and MCL1 are overexpressed in paclitaxel-resistant compared to paclitaxel-sensitive TNBC cells. We hypothesized that MYC and MC
To assess the effects of endocrine-disrupting chemicals on the expression and activity of aromatase in the gonads of Bombina orientalis, a common amphibian, we intraperitoneally injected nonylphenol or bisphenol-A and then examined aromatase mRNA levels by RT-PCR as well as aromatase enzymatic activity by tritiated water release assays. To design primers for the RT-PCR, we cloned the B. orientalis aromatase gene using RT-PCR and degenerate primers. The full-length cDNA was obtained by 5'- and 3'
Extracellular matrix protein 1 (ECM1) is associated with a poor prognosis of breast cancers. However, the role of ECM1 with endocrine resistance in estrogen receptor-positive (ER+) breast cancers has not been elucidated yet. We show that ECM1 promotes endocrine resistance in ER+ breast cancers. ECM1 is overexpressed in luminal breast cancer patients compared to the basal type of breast cancer. Significantly, higher expression of ECM1 is associated with poor response to endocrine therapies in lum
In 2015, there was a Middle East respiratory syndrome (MERS) outbreak in Korea. Interestingly, most of the cases were nosocomial infection and significant numbers of healthcare workers (HCWs) were infected. There were various causes, but this study focused on HCWs and their ability to self-protect from infectious materials. HCWs did not receive sufficient instruction or training on biosafety, including how to use personal protection equipment and risk assessment at the beginning of the outbreak.