Sujin Lee
Ewha Womans University · Medicine
About the Lab
Professor Sujin Lee's research lab focuses on molecular diagnostics and translational biomedical research, with a strong emphasis on identifying and validating biomarkers for early disease detection and therapeutic intervention. The lab specializes in developing advanced biosensing technologies—such as aptamer-based surface plasmon resonance platforms—for sensitive and label-free detection of disease-related proteins. Key research directions include understanding the role of matrix metalloproteinases in viral pathogenesis (e.g., HSV-induced corneal angiogenesis), investigating the molecular mechanisms of progeria and laminopathies, and exploring tumor microenvironment and metastatic patterns in cancers like colorectal and breast cancer. The lab integrates molecular biology, biochemistry, and nanobiosensors to uncover novel therapeutic targets and improve clinical outcomes.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Retinol binding protein 4 (RBP4) is a useful biomarker in the diagnosis of type 2 diabetes since its level in the serum is higher in insulin-resistant states. Accurate measurement of the serum RBP4 levels is hampered by conventional immunologic methods, such as enzyme-linked immunosorbent assay (ELISA). In this study, therefore, we have developed an aptamer-based surface plasmon resonance (SPR) biosensor that can be used to sense for RBP4 in serum samples. A single-stranded DNA (ssDNA) aptamer t
In this report, we demonstrate that herpes simplex virus (HSV) infection of the cornea results in the upregulation of the matrix-degrading metalloproteinase enzyme MMP-9. This enzyme was shown to contribute to the neovascularization process that occurs in the corneal stroma in response to HSV infection. The likely source of MMP-9, at least initially after infection, was neutrophils that were signaled to invade the cornea soon after infection. Corneal infiltrating neutrophils were shown to expres
Inc. (Indianapolis,
Hutchinson-Gilford progeria syndrome (HGPS) is a rare autosomal dominant genetic disease that is caused by a silent mutation of the LMNA gene encoding lamins A and C (lamin A/C). The G608G mutation generates a more accessible splicing donor site than does WT and produces an alternatively spliced product of LMNA called progerin, which is also expressed in normal aged cells. In this study, we determined that progerin binds directly to lamin A/C and induces profound nuclear aberrations. Given this
Breast cancer patients with "bone-only metastases" had excellent clinical outcomes. Further study is now warranted to reveal the underlying biology that regulates the behavior of this indolent tumor, as it should identify 'favorable tumor characteristics' in addition to 'favorable preferential metastatic site.'
c-MET overexpression, which was detected in 39 CRC patients (15.3%) irrespective of primary sites or molecular markers, indicated a poor survival prognosis and predicted shorter PFS during bevacizumab treatment in patients with CRC. Further studies are warranted to elucidate the value of c-MET-targeted therapy in CRC patients.
BACKGROUND: KIT has been suggested to be a potential therapeutic target for malignant melanoma. We evaluated the antitumor activity and safety of the KIT inhibitor nilotinib in metastatic melanoma patients harboring KIT gene mutations or amplifications. METHODS: We conducted a phase II multicenter trial of nilotinib in metastatic malignant melanoma with KIT mutations or amplifications. Patients received 400 mg oral nilotinib twice daily. The primary endpoint was response rate, and if seven or mo
BACKGROUND: c-N-Methyl-N'-nitro-N-nitroso-guanidine HOS transforming gene (c-MET) is a new potential drug target for treatment of patients with hepatocellular carcinoma (HCC), and a recent study of a c-MET inhibitor in such patients has shown promising results. In the present study, we investigated the incidence of c-MET overexpression and its prognostic impact. MATERIALS AND METHODS: Tumor tissue microarrays were used to detect the expression of c-MET in samples from 287 patients with HCC who u
본 연구에서는 기업의 사회적 책임(Corporate Social Responsibility, 이하 CSR)활동에 대한 종업원의 정당성 인식이이들의 조직시민행동이나 반생산적 과업활동에 미치는 영향에 대해 살펴본다. 정당성의 개념은 외재적 정당성과 내재적정당성으로 나누어지는데, 종업원이 기업조직에서 CSR활동에 치중하는 이유를 장기적인 경제적 이득이나 경쟁력향상의일환으로 귀인할 경우에는 외재적 정당성이 발생하는 반면, 조직의 비전을 구현하기 위한 일환으로 귀인할 경우에는 내재적 정당성이 발생하게 된다. 본 연구에서는 종업원이 기업조직의 CSR활동을 외재적 정당성보다 내재적 정당성에 귀인할경우, 이들의 조직시민행동은 증가하나, 조직내 반생산적 과업활동은 감소하는 것으로 예측하고 있다. 또한, 본 연구에서는 CSR활동에 대한 종업원의 냉소주의가 정당성과 종업원행동간의 관계를 매개한다고 예측하고 있다. 본 연구에서는 이러한 주장을 검증하기 위하여 DJSI KOREA 2009에 선정된 최우수기
BACKGROUND: Statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are commonly prescribed because of their therapeutic and preventive effects on cardiovascular diseases. Even though they have been occasionally reported to have antitumour activity, it is unknown whether statins have anti-angiogenic effect in human colorectal cancer (CRC). METHODS: A total of 11 human CRC cell lines were used to test the effects of bevacizumab, statins, and bevacizumab plus statins on human umbilica
TrkA IHC is an effective, initial screening method for NTRK1 rearrangement detection in the clinic. Inhibition of the TrkA kinase is a promising targeted therapy for cancer patients whose tumors harbor a NTRK1 rearrangement.
The combination of chemotherapy with chemosensitizing agents is a common approach to enhance anticancer activity while reducing the dose-dependent adverse side effects of cancer treatment. Herein, we investigated doxorubicin (DOX) and O-GlcNAc transferase (OGT) inhibitor OSMI-1 combination treatment, which significantly enhanced apoptosis in hepatocellular carcinoma cells (HepG2) as a result of synergistic drug action in disparate stress signaling pathways. Treatment with a low dose of DOX or a
Research Areas
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