详情页 - 首都医科大学宣武医院知识库

当前位置：首页 > 详情页

ADAM8 promotes chondrosarcoma cell migration and invasion by activating the NF-kappa B/MMP-13 signaling axisE

109| 导出 | 链接全文 |

文献详情

资源类型：

WOS体系：

Pubmed体系：

收录情况： ◇ SCIE

作者：

机构： [a]Department of Orthopaedic, Xuanwu Hospital Capital Medical University, [b]Beijing Northern Hospital of Weaponry Industry, Beijing [c]Department of Orthopaedic, Inner Mongolia BaoGang Hospital, The Third Affiliated Hospital of Inner Mongolia Medical University, Baotou, People’s Republic of China

出处：

DOI：

ISSN：

关键词： ADAM8 chondrosarcoma migration and invasion MMP-13 NF-kappa B

摘要：

ADAM8 is reported to promote extracellular matrix degradation to provide conditions for tumor metastasis. However, the underlying mechanism of ADAM8 in modulating chondrosarcoma (CHS) metastasis remains unclear. We used two human CHS cell lines SW1353 and HCS-2/8 to analyze the expression profiles of ADAM8 in CHS cells compared with the normal chondrocytes. An important proteolytic enzyme MMP-13 was detected as a marker for extracellular matrix degradation in chondrocytes. Then, by silencing or overexpressing ADAM8, the effects on cell migration and invasion in SW1353 and HCS-2/8, and the downstream signal transduction pathways were evaluated. ADAM8 and MMP-13 were highly expressed, and the NF-kappa B pathway was activated in SW1353 and HCS-2/8 cells. Silencing ADAM8 significantly reduced the ability of cell migration and invasion, and blocked the NF-kappa B signaling pathway through I kappa B alpha and p65 dephosphorylation, leading to reduced NF-kappa B transcription activity and decreased MMP-13 expression. ADAM8 overexpression promoted these processes, which, however, were reversed by an inhibitor Bay 11-7085. Our data showed a novel regulation mechanism for ADAM8 in promoting CHS migration and invasion by activating the NF-kappa B/MMP-13 signaling axis. Modulation of their levels may serve as potential targets in the treatment of CHS and even other cartilage diseases. Copyright (C) 2019 Wolters Kluwer Health, Inc. All rights reserved.

基金：

语种：

被引次数：

WOS：

PubmedID：

中科院(CAS)分区：

出版当年[2018]版：

大类 | 4 区医学

小类 | 4 区肿瘤学 4 区药学

最新[2023]版：

大类 | 4 区医学

小类 | 4 区肿瘤学 4 区药学

JCR分区：

出版当年[2017]版：

Q3 PHARMACOLOGY & PHARMACY Q4 ONCOLOGY

最新[2023]版：

Q3 ONCOLOGY Q3 PHARMACOLOGY & PHARMACY

影响因子： 1.8 最新[2023版] 1.9 最新五年平均 1.869 出版当年[2017版] 1.952 出版当年五年平均 2.32 出版前一年[2016版] 1.801 出版后一年[2018版]

第一作者：

第一作者机构： [a]Department of Orthopaedic, Xuanwu Hospital Capital Medical University, [c]Department of Orthopaedic, Inner Mongolia BaoGang Hospital, The Third Affiliated Hospital of Inner Mongolia Medical University, Baotou, People’s Republic of China

通讯作者：

通讯机构： [a]Department of Orthopaedic, Xuanwu Hospital Capital Medical University, [*1]Department of Orthopaedic, Xuanwu Hospital Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing 100053, People’s Republic of China

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]ADAM8 promotes chondrosarcoma cell migration and invasion by activating the NF-κB/MMP-13 signaling axis. [2]Suppression of NF-kappa B Reduces Myocardial No-Reflow [3]Cisplatin up-regulates ICAM-1 expression in endothelial cell via a NF-kappa B dependent pathway [4]SiRNA directed against NF-kappa B inhibits mononuclear macrophage cells releasing proinflammatory cytokines in vitro [5]Diabetes Activates Periodontal Ligament Fibroblasts via NF-kappa B In Vivo [6]NF-kappa B mediated Up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia [7]Oxymatrine induces nasopharyngeal cancer cell death through inhibition of PI3K/AKT and NF-kappa B pathways [8]Schisandrin B improves cerebral ischemia and reduces reperfusion injury in rats through TLR4/NF-kappa B signaling pathway inhibition [9]miR-181d/MALT1 regulatory axis attenuates mesenchymal phenotype through NF-kappa B pathways in glioblastoma [10]Aspirin inhibits LPS-induced macrophage activation via the NF-kappa B pathway