Eun Young Park

Korea Institute of Science and Technology, Sŏul, Seoul, South Korea

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Publications (144)260.67 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Human breast cancers include cancer stem cell populations as well as non-tumorigenic cancer cells. Breast cancer stem cells have self-renewal capability and are resistant to conventional chemotherapy. MicroRNAs (miRNAs) regulate the expression of many target genes; therefore, dysregulation of miRNAs have been associated with the pathogenesis of human diseases, including cancer. However, a role for miRNA dysregulation in stemness and drug resistance has yet to be identified. Members of the miR-34 family are reportedly tumor-suppressor miRNAs and are associated with various human cancers. Our results confirm that miR-34a expression was downregulated in MCF7/ADR cells compared with MCF7 cells. We hypothesized that this reduction was due to the p53 (TP53) mutation in MCF7/ADR cells. In this study, we found that primary and mature miR-34a were suppressed by treatment with p53 RNAi or the dominant negative p53 mutant in MCF7 cells. Ectopic miR-34a expression reduced cancer stem cell properties and increased sensitivity to doxorubicin treatment, by directly targeting NOTCH1. Furthermore, tumors from nude mice treated with miR-34a were significantly smaller compared to those of mice treated with control lentivirus. Our research suggests that the ectopic expression of miR-34a represents a novel therapeutic approach in chemoresistant breast cancer treatment.
    Cancer research. 11/2014;
  • Myungsun Yi, Keeho Park, Eun Young Park
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    ABSTRACT: The purpose of the study was to investigate significant psychosocial needs of low-income people with cancer in Korea and the extent to which these needs are unmet and which factors influence them.
    European journal of oncology nursing: the official journal of European Oncology Nursing Society 10/2014; · 1.13 Impact Factor
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    ABSTRACT: Excessive reactive oxygen species (ROS) production plays a crucial role in causing various diseases, including inflammatory disorders. The activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-κB) signaling is implicated in stimulating inflammatory response and cytokines. Peroxiredoxin 2 (Prx2) is a 2-cysteine (Cys) peroxiredoxin capable of removing endogenous hydrogen peroxide (H2O2). PEP-1 peptide, a protein transduction domain, consists of three domains which are used to transduce exogenous therapeutic proteins into cells. The correlation between effectively transduced PEP-1-Prx2 and ROS-mediated inflammatory response is not clear. In the present study, we investigated the protective effects of cell permeable PEP-1-Prx2 on oxidative stress-induced inflammatory activity in Raw 264.7 cells and in a mouse ear edema model after exposure to lipopolysaccharides (LPS) or 12-O-tetradecanoylphorbol-13-actate (TPA). Transduced PEP-1-Prx2 suppressed intracellular ROS accumulation and inhibited the activity of MAPKs and NF-κB signaling that led to the suppression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and cytokines in LPS-induced Raw 264.7 cells and TPA-induced mouse ear edema model. Given these results, we propose that PEP-1-Prx2 has therapeutic potential in the prevention of inflammatory disorders.
    International immunopharmacology. 09/2014;
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    ABSTRACT: Porphyrias are inherited metabolic disorders resulting from a specific enzyme defect in the heme biosynthetic pathway. Porphyrias are induced by various precipitants. Clinical features include abdominal pain, neurologic manifestations, autonomic neuropathy, and mental disturbance. Diagnosis may be delayed because of variable symptoms that mimic other diseases and because of the rarity of of porphyrias. Although most patients with known porphyria can complete anesthesia and surgery safely, undiagnosed porphyric patients are in danger of porphyric crisis due to inadvertent exposure to precipitating drugs and environment. We report a case of a patient who experienced delayed emergence with neurological disturbance after general anesthesia, ultimately diagnosed as acute intermittent porphyria.
    Korean journal of anesthesiology. 09/2014; 67(3):217-20.
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    ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by abnormal proliferation of renal tubular epithelial cells resulting in loss of renal function. Despite identification of the genes responsible for ADPKD, few effective drugs are currently available for the disease. Thus, finding additional effective drug targets is necessary. The functions of MRP3 have been reported only in the field of drug-resistance, and the renal functions of multidrug-resistance associated protein 3 (MRP) are mostly unknown. In this study, we found that MRP3 was significantly downregulated in kidneys of human patients with ADPKD and polycystic kidney disease (PKD) mouse models. Our results suggest that downregulated MRP3 stimulated renal epithelial cell proliferation through the B-Raf/MEK/ERK signaling pathway. In contrast, we found that restoring MRP3 reduced cell proliferation and cystogenesis in vitro. These results suggest that the renal function of MRP3 is related to renal cell proliferation and cyst formation and that restoring MRP3 may be an effective therapeutic approach for PKD.
    American journal of physiology. Renal physiology 08/2014; · 3.61 Impact Factor
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    ABSTRACT: The recent proliferation of data on large collections of well-characterized cancer cell lines linked to therapeutic drug responses has made it possible to identify lineage- and mutation-specific transcriptional markers that can help optimize implementation of anticancer agents. Here we leverage these resources, to systematically investigate the presence of mutation-specific transcription markers in a wide variety of cancer lineages and genotypes. Sensitivity and specificity of potential transcriptional biomarkers were simultaneously analyzed in 19 cell lineages grouped into 228 categories based on the mutational genotypes of 12 cancer-related genes. Among a total of 1,455 category-specific expression patterns, the expression of cAMP phosphodiesterase-4D (PDE4D) with 11 isoforms, one of the PDE4(A-D) sub-families, was predicted to be regulated by a mutant form of Serine/threonine kinase 11 (STK11)/liver kinase B1 (LKB1) present in lung cancer. STK11/LKB1 is the primary upstream kinase of adenine monophosphate-activated protein kinase (AMPK). Subsequently, we found that the knockdown of PDE4D gene expression inhibited proliferation of STK11-mutated lung cancer lines. Furthermore, challenge with a panel of PDE4 specific inhibitors was shown to selectively reduce the growth of STK11-mutated lung cancer lines. Thus we show that multidimensional analysis of a well-characterized large-scale panel of cancer cell lines provides unprecedented opportunities for identification of unexpected oncogenic mechanisms and mutation-specific drug targets.
    Molecular Cancer Therapeutics 08/2014; · 5.60 Impact Factor
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    ABSTRACT: Epithelial-mesenchymal transition (EMT) is associated with tumor hypoxia. EMT is regulated, in part, by the action of TWIST, which inhibits of E-cadherin expression and may interfere with the p53 tumor-suppressor pathway.
    The Korean Journal of Pathology 08/2014; 48(4):283-91. · 0.17 Impact Factor
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    ABSTRACT: Soft tissue sarcomas (STS) are rare. We evaluated the WT1 protein expression level in various types of STS and elucidated the value of WT1 as a prognostic factor and a possible therapeutic target.
    World Journal of Surgical Oncology 07/2014; 12(1):214. · 1.09 Impact Factor
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    ABSTRACT: We assessed the extent to which self-reported exposure to SHS underestimates the actual exposure to SHS and what factors are associated with a tolerance for SHS exposure in the Korean setting where the smoke-free policy is incomplete.
    Preventive medicine. 07/2014;
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    ABSTRACT: As it is known that FK506 binding proteins (FK506BPs) play an important role regulating a variety of biological processes for cell survival, this study was designed to examined the protective effects of FK506 binding protein 12 (FK506BP) on low humidity air flow induced dry eye in a rat model using transduced PEP-1-FK506BP. After the topically application of PEP-1-FK506BP tear volumes were markedly increased and cornea damage was significantly prevented compared with dry eye rats. Further, immunohistochemical analysis demonstrated that PEP-1-FK506BP markedly prevented damage to the cornea, the bulbar conjunctiva, and the palpebral conjunctiva epithelial lining compared with dry eye rats. Also this decreased caspase-3 and PARP expression levels. These results demonstrated that topically applied PEP-1-FK506BP significantly ameliorates dry eye injury in an animal model. Thus, we suggest that PEP-1-FK506BP can be developed as a new ophthalmic drop to treat dry eye diseases.
    BMB reports 07/2014; · 1.63 Impact Factor
  • Eun‐Young Park, Su‐Jung Nam
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    ABSTRACT: This study compares the digital literacy of people with and without disabilities in Korea, using data from the 2011 Information Divide Index Data of the National Information Society Agency (NIA). We extracted Internet and smart device users from the NIA samples and examined the main effects of disability, gender and age, as well as their interaction effects on Internet and smart device use and production literacy. Of the 1500 public individuals examined, 1190 (79.3%) were Internet users and 535 (35.7%) were smart device users. Of the 5300 with disabilities, 2110 (63.9%) were Internet users and 324 (8.8%) were smart device users. Generalized linear modelling showed significant main effects of disability, gender, age and education on Internet use and production literacy. The disability × age and disability × education interaction effects on Internet use literacy were statistically significant. We also observed a significant disability × age interaction effect on Internet production literacy. However, the main and interaction effects of disability, gender and education on smart device use and production literacy were not significant.
    International IJC 06/2014; · 0.66 Impact Factor
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    ABSTRACT: To develop effective intervention programmes to control Clonorchis sinensis infection, three interventions were evaluated in a clonorchiasis-endemic area of Korea.
    Tropical Medicine & International Health 05/2014; · 2.94 Impact Factor
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    ABSTRACT: AimAutosomal dominant polycystic kidney disease (ADPKD) is a highly prevalent inherited disorder and results in the progressive development of cysts in both kidneys. In recent studies, several cytokines and growth factors secreted by the cyst-lining epithelia were identified to be up-regulated and promote cyst growth. According to our previous study, chemokines with a similar amino acid sequence as human IL-8 are highly expressed in a rodent model with renal cysts. Therefore, in this study, we focused on whether IL-8 signaling is associated with renal cyst formation, and tested the possibility of IL-8 as a new therapeutic target for ADPKD.Methods Expression of IL-8 and its receptor were screened either by ELISA or western blot. Inhibited IL-8 signaling by antagonist for IL-8 receptor or gene silencing was tested in molecular levels, mainly through Western blot. And cell proliferation was measured by XTT assays. Finally, a three-dimensional culture was performed to understand how IL-8 affected cyst formation, in vitro.ResultsIL-8 secretion and expression of its receptor highly increased in 2 different human ADPKD cell lines (WT9-7 and WT9-12), compared to normal human renal cortical epithelial cell line. Cell proliferation which is mediated by IL-8 signal was inhibited either by an antagonist or siRNA targeting for IL-8 receptor. Finally, a three-dimensional culture showed an alleviation of cystogenesis in vitro, after blocking the IL-8 receptor signals.Conclusion These results suggest that IL-8 and its signaling molecules could be new biomarkers and a therapeutic target of ADPKD.
    Nephrology 04/2014; · 1.69 Impact Factor
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    ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited renal disorder. Although a myriad of research groups have attempted to identify a new therapeutic target for ADPKD, no drug has worked well in clinical trials. Our research group has focused on the receptor for advanced glycation end products (RAGE) gene as a novel target for ADPKD. This gene is involved in inflammation and cell proliferation. We have already confirmed that blocking RAGE function attenuates cyst growth in vitro. Based on this previous investigation, our group examined the effect of RAGE on cyst enlargement in vivo. PC2R mice, a severe ADPKD mouse model that we generated, were utilized. An adenovirus containing anti-RAGE shRNA was injected intravenously into this model. We observed that RAGE gene knockdown resulted in loss of kidney weight and volume. Additionally, the cystic area that originated from different nephron segments decreased in size due to downregulation of the RAGE gene. Blood urea nitrogen and creatinine values tended to be lower after inhibiting RAGE. Based on these results, we confirmed that the RAGE gene could be an effective target for ADPKD treatment.
    Journal of Biological Chemistry 02/2014; · 4.65 Impact Factor
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    ABSTRACT: Paraoxonase 1 (PON1) is an antioxidant enzyme which plays a central role in various diseases. However, the mechanism and function of PON1 protein in inflammation are poorly understood. Since PON1 protein alone cannot be delivered into cells, we generated a cell permeable PEP-1-PON1 protein using protein transduction domains, and examined whether it can protect against cell death in lipopolysaccharide (LPS) or hydrogen peroxide (H2O2)-treated Raw 264.7 cells as well as mice with 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced skin inflammation. We demonstrated that PEP-1-PON1 protein transduced into Raw 264.7 cells and markedly protected against LPS or H2O2-induced cell death by inhibiting cellular reactive oxygen species (ROS) levels, the inflammatory mediator's expression, activation of mitogen-activated protein kinases (MAPKs) and cellular apoptosis. Furthermore, topically applied PEP-1-PON1 protein ameliorates TPA-treated mice skin inflammation via a reduction of inflammatory response. Our results indicate that PEP-1-PON1 protein plays a key role in inflammation and oxidative stress in vitro and in vivo. Therefore, we suggest that PEP-1-PON1 protein may provide a potential protein therapy against oxidative stress and inflammation.
    PLoS ONE 01/2014; 9(1):e86034. · 3.53 Impact Factor
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    ABSTRACT: In nature, there exist a wide repertoire of dsRNA-binding proteins that have different binding modes for siRNA as well as structural differences, and some of these proteins have the potential as the effective siRNA delivery carriers. For delivering siRNA into cancer cells, a dsRNA-binding 2b protein derived from Tomato aspermy virus was genetically modified by fusing the integrin-targeting RGD peptide to its C-terminus, and biosynthesized. The resulting 2b-RGD protein possesses distinct characteristics favorable to biomedical applications of siRNA: (1) high affinity for siRNA, (2) siRNA protection against RNases in serum, (3) low cytotoxicity compared to the polycationic polymers often employed in the conventional siRNA carriers, (4) specific binding to integrins on cancer cells, and passing through the cell membrane via endocytosis, (5) ability to facilitate cytosolic release of siRNA. Here, we demonstrate the 2b-RGD/siRNA complexes have the high potential as a tumor-targeting siRNA delivery carrier and suggest their possible therapeutic applications for cancer treatment.
    Acta Biomaterialia. 01/2014;
  • Korean journal of anesthesiology 12/2013; 65(6 Suppl):S89-90.
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    ABSTRACT: We evaluated the performance, clinical role, and diagnostic accuracy of endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) in gastrointestinal intramural lesions. Procedural and pathologic data were reviewed from consecutive patients undergoing EUS-FNA for intramural lesions. Final diagnoses were determined by surgical histopathologic conformation and the diagnosis of malignancy, including clinical follow-up with repeat imaging. Forty-six patients (mean age, 47 years; 24 males) underwent EUS-FNA. Lesions were located in the stomach (n=31), esophagus (n=5), and duodenum (n=10). The median lesion size was 2 cm (range, 1 to 20.6). Final diagnoses were obtained in 22 patients (48%). EUS-FNA was diagnostic in 40 patients (87%). The diagnostic accuracy of cytology for differentiating between benign and malignant lesions was 82%; diagnostic error occurred in three patients (6%). The cytologic results influenced clinical judgment in 78% cases. The primary reasons for negative or no clinical impact were false-negative results, misdirected patient management, and inconclusive cytology. EUS-FNA exhibited an 87% diagnostic yield for gastrointestinal intramural lesions; the accuracy of cytology for differentiating malignancy was 82%. The limitations of EUS-FNA were primarily because of nondiagnostic sampling (9%) and probable diagnostic error (6%); these factors may influence the clinical role of EUS-FNA.
    Clinical endoscopy. 11/2013; 46(6):627-32.
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    ABSTRACT: Aging-dependent physiological conditions are attributed to parenchymal structural changes to cellular functions in aged organisms. To understand these aging-dependent processes, we compared the glucose formation capacity of primary hepatocytes from young (4-month-old) and old (24-month-old) Fisher 344 rats. The primary hepatocytes from old rats showed a higher glucose output and a higher expression of the key gluconeogenesis-regulating enzyme, phosphoenol pyruvate carboxykinase (PEPCK), compared with those from the young animals. The in situ hybridization study showed increased PEPCK mRNA expression in the aged liver tissues. The livers from old rats showed loosened hexagonal hepatic lobular structures, increased collagen accumulation, and high expression of the hypoxia marker hypoxia-inducible factor 1α (HIF1α). Hypoxia increased the PEPCK mRNA and protein expression levels in accordance with the HIF1α expression. PEPCK promoter luciferase reporter assay showed that hypoxia increased PEPCK through transcriptional activation. Furthermore, the Hepatocyte nuclear factor α (HNF4α) protein, but not the HNF4α mRNA level, increased in parallel with the PEPCK mRNA expression under hypoxic conditions. The glucose production increased in hypoxic condition, but this increment diminished by HNF4α siRNA in young hepatocytes. Moreover, increased glucose production from old rat hepatocytes was reversed by the down-regulation of HNF4α through a specific siRNA. This study suggests that the mild hypoxic conditions in response to aging-dependent hepatic structural changes may contribute to the induction of the gluconeogenic enzyme PEPCK through HNF4α protein stabilization.
    Experimental gerontology 10/2013; · 3.34 Impact Factor
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    ABSTRACT: We examined the ways in which fenobam could promote not only the transduction of PEP-1-FK506BP into cells and tissues but also the neuroprotective effect of PEP-1-FK506BP against ischemic damage. Fenobam strongly enhanced the protective effect of PEP-1-FK506BP against H2O2-induced toxicity and DNA fragmentation in C6 cells. In addition, combinational treatment of fenobam with PEP-1-FK506BP significantly inhibited the activation of Akt and MAPK induced by H2O2, compared to treatment with PEP-1-FK506BP alone. Interestingly, our results showed that fenobam significantly increased the transduction of PEP-1-FK506BP into both C6 cells and the hippocampus of gerbil brains. Subsequently, a transient ischemic gerbil model study demonstrated that fenobam pretreatment led to the increased neuroprotection of PEP-1-FK506BP in the CA1 region of the hippocampus. Therefore, these results suggest that fenobam can be a useful agent to enhance the transduction of therapeutic PEP-1-fusion proteins into cells and tissues, thereby promoting their neuroprotective effects.
    BMB reports 10/2013; · 1.63 Impact Factor

Publication Stats

1k Citations
260.67 Total Impact Points


  • 2014
    • Korea Institute of Science and Technology
      • Center for Theragnosis
      Sŏul, Seoul, South Korea
  • 2012–2014
    • Hallym University Medical Center
      • Department of Anesthesiology and Pain Medicine
      Sŏul, Seoul, South Korea
    • Pusan National University
      • Department of Surgery
      Pusan, Busan, South Korea
    • Konyang University
      • Department of Medicine
      Nonsan, South Chungcheong, South Korea
    • Chungnam National University
      • Department of Horticultural Science
      Daiden, Daejeon, South Korea
    • Ajou University
      • Department of Medicine
      Sŏul, Seoul, South Korea
  • 2011–2014
    • Jeonju University
      • Department of Secondary Special Education
      Sŏul, Seoul, South Korea
    • Ulsan College
      Urusan, Ulsan, South Korea
  • 2007–2014
    • Sookmyung Women's University
      • Department of Biological Science
      Sŏul, Seoul, South Korea
  • 2004–2014
    • National Cancer Center Korea
      Kōyō, Gyeonggi Province, South Korea
  • 2013
    • Kyungpook National University
      • Green-Nano Materials Research Center
      Daikyū, Daegu, South Korea
  • 2011–2013
    • Gachon University
      • • Department of Nursing (College of Nursing)
      • • Lee Gil Ya Cancer and Diabetes Institute
      Sŏngnam, Gyeonggi Province, South Korea
  • 2005–2013
    • Catholic University of Korea
      • Department of Urology
      Sŏul, Seoul, South Korea
    • Seoul National University Hospital
      • Department of Nuclear Medicine
      Sŏul, Seoul, South Korea
  • 2004–2013
    • Korea University
      • College of Nursing
      Sŏul, Seoul, South Korea
  • 2011–2012
    • Hallym University
      • College of Medicine
      Seoul, Seoul, South Korea
  • 2009–2011
    • Hannam University
      • Department of Advanced Materials
      Daiden, Daejeon, South Korea
    • Ewha Womans University
      • Department of Pediatrics
      Sŏul, Seoul, South Korea
  • 2010
    • Korea Institute of Radiological & Medical Sciences
      Sŏul, Seoul, South Korea
  • 2008
    • Chonnam National University
      • Department of Pediatrics
      Gwangju, Gwangju, South Korea
    • Dong Seoul College
      Sŏul, Seoul, South Korea
  • 2007–2008
    • Hanyang University
      • Division of Chemical Engineering and Bioengineering
      Sŏul, Seoul, South Korea
  • 2002–2008
    • Seoul National University
      • • Department of Preventive Medicine
      • • College of Pharmacy
      • • Research Institute of Pharmaceutical Sciences
      • • Department of Biological Sciences
      Sŏul, Seoul, South Korea
    • Hankuk University of Foreign Studies
      • Department of Bioscience and Biotechnology
      Sŏul, Seoul, South Korea