• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

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

慢病毒介导的 shRNA 敲低人骨肉瘤细胞中的 MED19 通过诱导 G0/G1 期细胞周期阻滞抑制细胞增殖。

Knockdown of MED19 by lentivirus-mediated shRNA in human osteosarcoma cells inhibits cell proliferation by inducing cell cycle arrest in the G0/G1 phase.

机构信息

Department of Orthopaedics, The First Hospital of Jilin University, Changchun, China.

出版信息

Oncol Res. 2011;19(5):193-201. doi: 10.3727/096504011x12970940207760.

DOI:10.3727/096504011x12970940207760
PMID:21542455
Abstract

MED 19 is a subunit of the mediator complex, which is a coactivator of RNA polymerase II and also interacts with the downstream coding region of many genes. However, the role of MED19 in osteosarcoma is unknown. In the present study, we applied lentivirus-mediated short hairpin RNA (shRNA)-triggered RNA interference to downregulate MED19 expression in human osteosarcoma SaOS-2 and U2OS cells. Knockdown of MED19 expression was confirmed by real-time PCR and Western blot. It was found that silencing of MED19 resulted in decreased cell viability, colony formation capacity, and DNA synthesis ability in both cells, as well as the G0/G1 phase cell cycle arrest. These results implied that MED19 played an important role in cell growth and cell cycle progression of human osteosarcoma cells. MED19 may be an attractive candidate for the therapeutic target in osteosarcoma.

摘要

MED19 是中介体复合物的一个亚基,它是 RNA 聚合酶 II 的共激活因子,也与许多基因的下游编码区相互作用。然而,MED19 在骨肉瘤中的作用尚不清楚。在本研究中,我们应用慢病毒介导的短发夹 RNA(shRNA)触发 RNA 干扰来下调人骨肉瘤 SaOS-2 和 U2OS 细胞中的 MED19 表达。通过实时 PCR 和 Western blot 验证了 MED19 表达的下调。结果发现,沉默 MED19 表达导致两种细胞的细胞活力、集落形成能力和 DNA 合成能力下降,以及 G0/G1 期细胞周期停滞。这些结果表明,MED19 在人骨肉瘤细胞的生长和细胞周期进程中发挥着重要作用。MED19 可能是骨肉瘤治疗靶点的一个有吸引力的候选物。

相似文献

1
Knockdown of MED19 by lentivirus-mediated shRNA in human osteosarcoma cells inhibits cell proliferation by inducing cell cycle arrest in the G0/G1 phase.慢病毒介导的 shRNA 敲低人骨肉瘤细胞中的 MED19 通过诱导 G0/G1 期细胞周期阻滞抑制细胞增殖。
Oncol Res. 2011;19(5):193-201. doi: 10.3727/096504011x12970940207760.
2
Knockdown of MED19 by short hairpin RNA-mediated gene silencing inhibits pancreatic cancer cell proliferation.短发夹 RNA 介导的基因沉默敲低 MED19 抑制胰腺癌细胞增殖。
Cancer Biother Radiopharm. 2011 Aug;26(4):495-501. doi: 10.1089/cbr.2010.0863.
3
Knockdown of mediator complex subunit 19 inhibits the growth of ovarian cancer.敲低中介体复合物亚基 19 抑制卵巢癌细胞生长。
Mol Med Rep. 2012 Nov;6(5):1050-6. doi: 10.3892/mmr.2012.1065. Epub 2012 Sep 5.
4
Mediator of RNA polymerase II transcription subunit 19 promotes osteosarcoma growth and metastasis and associates with prognosis.RNA 聚合酶 II 转录亚基 19 介体促进骨肉瘤生长和转移,并与预后相关。
Eur J Cancer. 2014 Apr;50(6):1125-36. doi: 10.1016/j.ejca.2014.01.030. Epub 2014 Feb 21.
5
Disruption of mediator complex subunit 19 (Med19) inhibits cell growth and migration in tongue cancer.中介体复合物亚基 19(Med19)的破坏抑制舌癌中的细胞生长和迁移。
World J Surg Oncol. 2013 May 27;11:116. doi: 10.1186/1477-7819-11-116.
6
Lentivirus-Mediated Knockdown of CTHRC1 Inhibits Osteosarcoma Cell Proliferation and Migration.慢病毒介导的CTHRC1基因敲低抑制骨肉瘤细胞增殖和迁移。
Cancer Biother Radiopharm. 2016 Apr;31(3):91-8. doi: 10.1089/cbr.2014.1758. Epub 2016 Apr 4.
7
Med19 promotes gastric cancer progression and cellular growth.Med19 促进胃癌进展和细胞生长。
Gene. 2012 Aug 10;504(2):262-7. doi: 10.1016/j.gene.2012.04.033. Epub 2012 Apr 28.
8
Antidifferentiation Noncoding RNA Regulates the Proliferation of Osteosarcoma Cells.反分化非编码RNA调控骨肉瘤细胞的增殖。
Cancer Biother Radiopharm. 2016 Mar;31(2):52-7. doi: 10.1089/cbr.2015.1888.
9
Expression of Med19 in bladder cancer tissues and its role on bladder cancer cell growth.Med19 在膀胱癌组织中的表达及其对膀胱癌细胞生长的作用。
Urol Oncol. 2012 Nov-Dec;30(6):920-7. doi: 10.1016/j.urolonc.2010.10.003. Epub 2011 Apr 7.
10
Lentivirus-mediated inhibition of Med19 suppresses growth of breast cancer cells in vitro.慢病毒介导的 Med19 抑制可抑制乳腺癌细胞的体外生长。
Cancer Chemother Pharmacol. 2011 Jul;68(1):207-15. doi: 10.1007/s00280-010-1468-9. Epub 2010 Oct 2.

引用本文的文献

1
Mediator Complex Subunit 19 Promotes the Development of Hepatocellular Carcinoma by Regulating the AKT/mTOR Signaling Pathway.中介体复合物亚基19通过调控AKT/mTOR信号通路促进肝细胞癌的发展。
Front Oncol. 2022 Jan 3;11:792285. doi: 10.3389/fonc.2021.792285. eCollection 2021.
2
microRNAs and Corresponding Targets Involved in Metastasis of Colorectal Cancer in Preclinical Models.miRNAs 及其在临床前模型中结直肠癌转移相关的靶基因。
Cancer Genomics Proteomics. 2020 Sep-Oct;17(5):453-468. doi: 10.21873/cgp.20204.
3
Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells.
钙结合蛋白1的下调会降低骨肉瘤细胞的增殖。
Oncol Lett. 2017 May;13(5):3727-3733. doi: 10.3892/ol.2017.5931. Epub 2017 Mar 28.
4
Knockdown of Mediator Complex Subunit 19 Suppresses the Growth and Invasion of Prostate Cancer Cells.中介体复合物亚基19的敲低抑制前列腺癌细胞的生长和侵袭。
PLoS One. 2017 Jan 26;12(1):e0171134. doi: 10.1371/journal.pone.0171134. eCollection 2017.
5
A large-scale RNAi screen identifies LCMR1 as a critical regulator of Tspan8-mediated melanoma invasion.大规模 RNAi 筛选鉴定 LCMR1 为 Tspan8 介导的黑色素瘤侵袭的关键调节因子。
Oncogene. 2017 Jan 26;36(4):446-457. doi: 10.1038/onc.2016.219. Epub 2016 Jul 4.
6
Drosophila melanogaster Hox transcription factors access the RNA polymerase II machinery through direct homeodomain binding to a conserved motif of mediator subunit Med19.果蝇的同源异型转录因子通过其同源结构域直接结合中介体亚基Med19的保守基序来接触RNA聚合酶II机制。
PLoS Genet. 2014 May 1;10(5):e1004303. doi: 10.1371/journal.pgen.1004303. eCollection 2014 May.
7
Gene expression profile of the whole Mediator complex in human osteosarcoma and normal osteoblasts.人骨肉瘤和正常成骨细胞中整个中介复合物的基因表达谱。
Med Oncol. 2013 Dec;30(4):739. doi: 10.1007/s12032-013-0739-9. Epub 2013 Oct 8.
8
Silencing SATB1 inhibits proliferation of human osteosarcoma U2OS cells.沉默 SATB1 抑制人骨肉瘤 U2OS 细胞的增殖。
Mol Cell Biochem. 2013 Jun;378(1-2):39-45. doi: 10.1007/s11010-013-1591-0. Epub 2013 Mar 21.