Suppr超能文献

双特异性磷酸酶1抑制胆囊癌中的细胞增殖、转移、侵袭和血管生成。

DUSP1 inhibits cell proliferation, metastasis and invasion and angiogenesis in gallbladder cancer.

作者信息

Shen Jiliang, Zhou Senjun, Shi Liang, Liu Xiaolong, Lin Hui, Yu Hong, Tang Jiacheng, Yu Tunan, Cai Xiujun

机构信息

Department of General Surgery, Sir Run-Run Shaw Hospital, Zhejiang University, Hangzhou 310016, China.

出版信息

Oncotarget. 2017 Feb 14;8(7):12133-12144. doi: 10.18632/oncotarget.14815.

Abstract

DUSP1/MKP1 is a dual-specific phosphatase that regulates MAPK activity and is known to play a key role in tumor biology. Its function in gallbladder cancer (GBC) remains largely unknown, however. By exploring its activities in two GBC cell lines (SGC996 and GBC-SD), DUSP1 was found to inhibit GBC cell proliferation, migration and invasion. Moreover, DUSP1 inhibited GBC growth and metastasis in nude mice subcutaneously xenografted with SGC996 cells. The tumor suppression appeared to be mediated via the DUSP1-pERK/MAPK-MMP2 signal pathway. Angiogenesis was associated with the tumor metastasis in the mouse model and was impaired by DUSP1, which suppressed VEGF expression. These results suggest that DUSP1 suppresses GBC growth and metastasis by targeting the DUSP1-pERK-MMP2/VEGF axis. Identification of the DUSP1-pERK-MMP2/VEGF signals may provide new biomarkers and/or therapeutic targets to better suppress GBC metastasis in the future.

摘要

双特异性磷酸酶1(DUSP1)/丝裂原活化蛋白激酶磷酸酶1(MKP1)是一种双特异性磷酸酶,可调节丝裂原活化蛋白激酶(MAPK)的活性,并且已知在肿瘤生物学中起关键作用。然而,其在胆囊癌(GBC)中的功能仍 largely 未知。通过探索其在两种GBC细胞系(SGC996和GBC-SD)中的活性,发现DUSP1可抑制GBC细胞的增殖、迁移和侵袭。此外,DUSP1抑制了皮下接种SGC996细胞的裸鼠体内GBC的生长和转移。肿瘤抑制似乎是通过DUSP1-pERK/MAPK-MMP2信号通路介导的。在小鼠模型中,血管生成与肿瘤转移相关,并且被抑制VEGF表达的DUSP1所损害。这些结果表明,DUSP1通过靶向DUSP1-pERK-MMP2/VEGF轴抑制GBC的生长和转移。鉴定DUSP1-pERK-MMP2/VEGF信号可能为未来更好地抑制GBC转移提供新的生物标志物和/或治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b066/5355331/a4e2f4c2cb4e/oncotarget-08-12133-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验