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Li Yi,Peng Feng,Tan Xiangyun,Wang Jin,Xu Yeqing 한국유전학회 2021 Genes & Genomics Vol.43 No.10
Background Colorectal cancer (CRC) exhibits high risks of morbidity and mortality. Objective To investigate the efect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development. Methods The SCRAR5 expression in four kinds of CRC cell lines (SW620, SW480, HT29, and HCT116) was measured by quantitative PCR and western blotting, respectively. The efects of SCRAR5 abnormal expression on cell proliferation, apoptosis, and migration were analyzed by CCK-8 assay, EdU assay, colony-forming assay, fow cytometry assay, Transwell assay and wound healing assay, respectively. Meanwhile, the involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo efects of SCRAR5 abnormal expression on CRC xenograft mice were fnally investigated by evaluating tumor volume, apoptosis and Ki67 expression. Results SCRAR5 was lowly expressed in CRC cell lines, especially SW480 cells. Up-regulation of SCRAR5 signifcantly promoted cell apoptosis, reduced cell proliferation and migration in SW480 cells. Notably, SCRAR5 overexpression obviously inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Reversely, SCRAR5 silence exhibited promoting efects on HT29 cells. Consistently, in vivo experiments also revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis. Conclusions Overall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway.
Chuanxian Jiang,Zhiping Li,Xiaohui Chen,Zejun Zhang,Yeqing Yi 보안공학연구지원센터 2016 International Journal of Smart Home Vol.10 No.9
This paper presents an efficient algorithm that segments the synthetic aperture radar (SAR) image into several homogeneous regions by combining edge- and region-based information. A multi-direction ratio edge detector is used to capture the locally directional variation information of a SAR image and construct the ratio edge strength map (RESM) of the SAR image. Watershed transformation is performed on the thresholded RESM to obtain an over-segmentation result. An efficient hierarchical region merging procedure based on the region adjacency graph representation of the image regions is proposed. A novel dissimilarity measurement between the two adjacent regions is derived from the multiplicative noise speckle model of the multi-look SAR image. Experimental results and the performance evaluation show that the proposed method outperforms two widely used SAR image segmentation approaches.
MicroRNA-409-3p Inhibits Migration and Invasion of Bladder Cancer Cells via Targeting c-Met
Xin Xu,Liping Xie,Hong Chen,Yiwei Lin,Zhenghui Hu,Yeqing Mao,Jian Wu,Xianglai Xu,Yi Zhu,Shiqi Li,Xiangyi Zheng 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.1
There is increasing evidence suggesting that dysregulation of certain microRNAs (miRNAs) may con-tribute to tumor progression and metastasis. Previous studies have shown that miR-409-3p is dysregulated in some malignancies, but its role in bladder cancer is still unknown. Here, we find that miR-409-3p is down-regulated in human bladder cancer tissues and cell lines. Enforced expression of miR-409-3p in bladder cancer cells significantly reduced their migration and invasion without affecting cell viability. Bioinformatics analysis identified the pro-metastatic gene c-Met as a potential miR-409-3p target. Further studies indicated that miR-409-3p suppressed the expression of c-Met by binding to its 3-untranslated region. Silencing of c-Met by small interfering RNAs phenocopied the effects of miR-409-3p overexpression, whereas restoration of c-Met in bladder cancer cells bladder cancer cells overexpressing miR-409-3p, partially reversed the suppressive effects of miR-409-3p. We further showed that MMP2 and MMP9 may be downstream effector proteins of miR-409-3p. These findings indicate that miR-409-3p could be a potential tumor suppressor in bladder cancer.
MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1
Liang, Zhen,Li, Shiqi,Xu, Xin,Xu, Xianglai,Wang, Xiao,Wu, Jian,Zhu, Yi,Hu, Zhenghui,Lin, Yiwei,Mao, Yeqing,Chen, Hong,Luo, Jindan,Liu, Ben,Zheng, Xiangyi,Xie, Liping Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.2
MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3'-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3'-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.
MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1
Liping Xie,Zhen Liang,Shiqi Li,Xin Xu,Xianglai Xu,Xiao Wang,Jian Wu,Yi Zhu,Zhenghui Hu,Yiwei Lin,Yeqing Mao,Hong Chen,Jindan Luo,Ben Liu,Xiangyi Zheng 한국분자세포생물학회 2015 Molecules and cells Vol.38 No.2
MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3 -UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3 -UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.