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      • KCI등재

        Benzidine Induces Epithelial-Mesenchymal Transition of Human Bladder Cancer Cells through Activation of ERK5 Pathway

        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.

      • KCI등재

        Benzidine Induces Epithelial–Mesenchymal Transition of Human Bladder Cancer Cells through Activation of ERK5 Pathway

        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.

      • SCOPUSKCI등재

        Block Sparse Signals Recovery via Block Backtracking-Based Matching Pursuit Method

        Qi, Rui,Zhang, Yujie,Li, Hongwei Korea Information Processing Society 2017 Journal of information processing systems Vol.13 No.2

        In this paper, a new iterative algorithm for reconstructing block sparse signals, called block backtracking-based adaptive orthogonal matching pursuit (BBAOMP) method, is proposed. Compared with existing methods, the BBAOMP method can bring some flexibility between computational complexity and reconstruction property by using the backtracking step. Another outstanding advantage of BBAOMP algorithm is that it can be done without another information of signal sparsity. Several experiments illustrate that the BBAOMP algorithm occupies certain superiority in terms of probability of exact reconstruction and running time.

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