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RISS 인기검색어
- 검색키워드
- 저자 : Zhang Qifei (검색결과 3 건)
- 무료
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- 유료
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Sun, Xin,Zhang, Tao,Deng, Qifei,Zhou, Qirui,Sun, Xianchao,Li, Enlai,Yu, Dexin,Zhong, Caiyun Korean Society for Molecular and Cellular Biology 2018 Molecules and cells Vol.41 No.3
Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial-mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker expression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was activated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.
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Research on the Efficiency of Cloud Resource Allocation and Operation Based on DEA Method
Li Wenjuan,Wu Jiyi,Zhang Qifei,Zhao Haili 보안공학연구지원센터 2015 International Journal of Grid and Distributed Comp Vol.8 No.5
In order to compensate for the current lack of assessing cloud resource allocation and business operation from the economical perspective, this paper introduced the Data Envelopment Analysis (DEA) method which is one of the most famous methods in economics into this field. Based on it, it proposed several new methods to evaluate the efficiency of cloud resource allocation and cloud providers’ business operation status through the way of case study.
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Xin Sun,Tao Zhang,Qifei Deng,Qirui Zhou,Xianchao Sun,Enlai Li,Dexin Yu,Caiyun Zhong 한국분자세포생물학회 2018 Molecules and cells Vol.41 No.3
Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial–mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker ex-pression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was acti-vated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.
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