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Kim, E-S,Cha, Y,Ham, M,Jung, J,Kim, S G,Hwang, S,Kleemann, R,Moon, A Macmillan Publishers Limited 2014 Oncogene Vol.33 No.27
A crucial role of the inflammatory lipid sphingosine-1-phosphate (S1P) in breast cancer aggressiveness has been reported. Recent clinical studies have suggested that C-reactive protein (CRP) has a role in breast cancer development. However, limited information is available on the molecular basis for the expression of CRP and its functional significance in breast cell invasion. The present study aimed to elucidate the molecular link between S1P and CRP during the invasive process of breast epithelial cells. This is the first report showing that transcription of CRP was markedly activated by S1P in breast cells. Our data suggest that not only S1P treatment but also the endogenously produced S1P may upregulate CRP in breast carcinoma cells. Transcription factors CCAAT/enhancer-binding protein beta and c-fos were required for S1P-induced CRP expression. Coupling of S1P<SUB>3</SUB> to heterotrimeric G<SUB>αq</SUB> triggered the expression of CRP, utilizing signaling pathways involving reactive oxygen species (ROS), Ca<SUP>2+</SUP> and extracellular signal-related kinases (ERKs). S1P-induced CRP expression was crucial for the transcriptional activation of matrix metalloproteinase-9 through ERKs, ROS and c-fos, leading to breast cell invasion. Using a xenograft mice tumor model, we demonstrated that S1P induced CRP expression both in vitro and in vivo. Taken together, our findings have revealed a molecular basis for S1P-induced transcriptional activation of CRP and its functional significance in the acquisition of the invasive phenotype of human breast epithelial cells under inflammatory conditions. Our findings may provide useful information on the identification of useful therapeutic targets for inflammatory breast cancer.
p34 is a novel regulator of the oncogenic behavior of NEDD4-1 and PTEN
Hong, S-W,Moon, J-H,Kim, J-S,Shin, J-S,Jung, K-A,Lee, W-K,Jeong, S-Y,Hwang, J J,Lee, S-J,Suh, Y-A,Kim, I,Nam, K-Y,Han, S,Kim, J E,Kim, K-p,Hong, Y S,Lee, J-L,Lee, W-J,Choi, E K,Lee, J S,Jin, D-H,Kim, Macmillan Publishers Limited 2014 CELL DEATH AND DIFFERENTIATION Vol.21 No.1
PTEN is one of the most frequently mutated or deleted tumor suppressors in human cancers. NEDD4-1 was recently identified as the E3 ubiquitin ligase for PTEN; however, a number of important questions remain regarding the role of ubiquitination in regulating PTEN function and the mechanisms by which PTEN ubiquitination is regulated. In the present study, we demonstrated that p34, which was identified as a binding partner of NEDD4-1, controls PTEN ubiquitination by regulating NEDD4-1 protein stability. p34 interacts with the WW1 domain of NEDD4-1, an interaction that enhances NEDD4-1 stability. Expression of p34 promotes PTEN poly-ubiquitination, leading to PTEN protein degradation, whereas p34 knockdown results in PTEN mono-ubiquitination. Notably, an inverse correlation between PTEN and p34/NEDD4-1 levels was confirmed in tumor samples from colon cancer patients. Thus, p34 acts as a key regulator of the oncogenic behavior of NEDD4-1 and PTEN.
Park, S. J.,Kim, S. M.,Moon, J. H.,Kim, J. H.,Shin, J. S.,Hong, S. W.,Shin, Y. J.,Lee, D. H.,Lee, E. Y.,Hwang, I. Y. Springer Science + Business Media 2016 Tumour biology Vol.37 No.4
<P>Pancreatic cancer is one of the most lethal cancers and remains a major unsolved health problem. Less than 20 % of patients are surgical candidates, and the median survival for non-resected patients is approximately 3 to 4 months. Despite the existence of many conventional cancer therapies, few targeted therapies have been developed for pancreatic cancer. Combination therapy using erlotinib and gemcitabine is an approved standard chemotherapy for advanced pancreatic cancer, but it has marginal therapeutic benefit. To try to improve the therapeutic outlook, we studied the efficacy of another combination treatment and the relevance to E-cadherin in human pancreatic cancer cells. We treated two human pancreatic cancer cell lines with the histone deacetylase inhibitor (HDACi) SAHA. Interestingly, in these Panc-1 and Capan1 cells, we observed that the expression levels of E-cadherin and phosphorylated EGFR were gradually upregulated after treatment with SAHA. Furthermore, these cells underwent induced cell death after exposure to the combination treatment of SAHA and erlotinib. In Panc-1 cells, overexpression of E-cadherin activated the phosphorylation of EGFR and increased the cell sensitivity to erlotinib. In Capan1 cells, knocking down E-cadherin decreased the expression of phosphorylated EGFR, and these cells did not respond to erlotinib. Therefore, we demonstrated the efficacy of the combined treatment with SAHA and erlotinib in human pancreatic cancer cells, and we determined that the increased efficacy was due, at least in part, to the effects of SAHA on the expression of E-cadherin. Our studies suggest that E-cadherin may be a potent biomarker for pancreatic cancer.</P>
Chung, C.,Yoo, G.,Kim, T.,Lee, D.,Lee, C.S.,Cha, H.R.,Park, Y.H.,Moon, J.Y.,Jung, S.S.,Kim, J.O.,Lee, J.C.,Kim, S.Y.,Park, H.S.,Park, M.,Park, D.I.,Lim, D.S.,Jang, K.W.,Lee, J.E. Academic Press 2016 Biochemical and biophysical research communication Vol.479 No.2
Somatic mutation in the tyrosine kinase domain of epidermal growth factor receptor (EGFR) is a decisive factor for the therapeutic response to EGFR tyrosine kinase inhibitors (EGFR-TKIs) in lung adenocarcinoma. The stability of mutant EGFR is maintained by various regulators, including heat shock protein 90 (Hsp90). The C terminus of Hsc70-interacting protein (CHIP) is a Hsp70/Hsp90 co-chaperone and exhibits E3 ubiquitin ligase activity. The high-affinity Hsp90-CHIP complex recognizes and selectively regulates their client proteins. CHIP also works with its own E3 ligase activity independently of Hsp70/Hsp90. Here, we investigated the role of CHIP in regulating EGFR in lung adenocarcinoma and also evaluated the specificity of CHIP's effects on mutant EGFR. In HEK 293T cells transfected with either WT EGFR or EGFR mutants, the overexpression of CHIP selectively decreased the expression of certain EGFR mutants (G719S, L747_E749del A750P and L858R) but not WT EGFR. In a pull-down assay, CHIP selectively interacted with EGFR mutants and simultaneously induced their ubiquitination and proteasomal degradation. The expressions of mutant EGFR in PC9 and H1975 were diminished by CHIP, while the expression of WT EGFR in A549 was nearly not affected. In addition, CHIP overexpression inhibited cell proliferation and xenograft's tumor growth of EGFR mutant cell lines, but not WT EGFR cell lines. EGFR mutant specific ubiquitination by CHIP may provide a crucial regulating mechanism for EGFR in lung adenocarcinoma. Our results suggest that CHIP can be novel therapeutic target for overcoming the EGFR TKI resistance.
Fabrication and Atmospheric Pressure Dependent Electrical Properties of the ZnO Nanowire Device
E.-K Kim,S. E. Moon,G. T. Kim,H. J. Ji,H.-Y. Lee,J. Park,J. H. Kwak,K.-H. Park,S. Maeng,S. J. Park,S.-W. Kim 한국물리학회 2007 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.51 No.II
A single ZnO nanowire device was fabricated by electron-beam lithography, and its current-voltage characteristics were recorded while varying the atmospheric pressure to test possible applications as a chemical gas sensor. Vertically well aligned ZnO nanowires were grown on GaN epilayer on c-plane sapphire {\it via} a vapor-liquid-solid (VLS) process by introducing an Au thin film (3 nm) as a catalyst. Semiconducting nanowire devices were fabricated by using photolithography and e-beam lithography, and their electrical properties were studied. To realize reliable device operation, which is a key factor for a chemical sensor, the contact resistance should be optimized. Here, we studied the contact-resistance problem by using a scanning probe microscopic tool to characterize surface-potential behaviors. To overcome the contact-resistance problem, a post thermal process was adapted to the nanowire device. Atmospheric-pressure-dependent electrical properties of the ZnO nanowire device were studied for chemical-sensor application.
2001년 11월 오염시기와 2002년 봄 황사시기 제주도 고산에서의 미량원소 농도 변화
한진석,김영성,문광주,안준영,김정은,류성윤,김영준,공부주,이석조 한국대기환경학회 2004 한국대기환경학회지 Vol.20 No.2
The chemical composition of PM_(2.5) was measured at Gosan. Jeju for two weeks each in November 2001 and spring 2002. In the latter part of the measurement period of November 2001, designated as the polluted period in this work, secondarily formed ion components as well as primarily emitted elemental carbon were high, PM_(2.5) mass concentration was also high in this polluted period compared with the yellow sand period, in which daily average of PM_(10) peaked up to 520㎍/㎥. Increase of major components of anthropogenic origin in the polluted period was not correlated with the variation in sea salt components while increase of crustal components in the yellow sand period was highly correlated with the variation in sea salt components. Trace elements were generally higher in the yellow sand period: however, toxic heavy metals such as zinc, cadmium and lead were the highest in the polluted period.
대학생의 취침 전 스마트폰 사용과 수면의 질 간의 관계
김보민,김지은,김희진,문소연,문재민,송지원,양다경,이서연,정유담,허혜빈,배성희 이화여자대학교간호학회 2020 이화간호학회지 Vol.- No.54
Purpose: This study's main objectives are to examine the relationship of smartphone use at bedtime and sleep quality among college students. Methods: A sample 189 Korean college students(20-26 years old( participated in a survey about smartphone use in bed time and sleep quality. Self-reported sleep quality, daytime fatigue and insomnia were measured using the Pittsburgh Sleep Quality Index Korean version (PSQI-K). There are 3 sections of the questionnaire; 1) general information 2) sleep quality using PSQI-K 3) smartphone usage before bedtime. Data was analyzed using cross tabulation, one-way ANOVA, and independent T-Test. Results: 1. There was a difference whether they suffer from daily life due to the use of smartphones before bedtime between college student‘s sex and majors. 2. There was a difference in the main purpose of using smartphone before bedtime by age. 3. Respondents who used their smartphones before bedtime everyday showed prolonged sleep latency than those who used smartphones before bedtime less frequently. 4. There was no significant difference in the quality of sleep according to usage time and recognition on smartphone usage before bedtime and its disturbance of daily life. 5. The quality of sleep according to the purpose of smartphone usage before bedtime showed no significant difference. Conclusion: Based on the study results, there is the necessity of self-management among college students to enhance their sleep quality. Additionally, further research on the smartphone usage before bedtime is necessary due to the absence of the precedent studies and gender imbalance in the collected data.