• 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

CIP2A,一种癌蛋白,与喉癌细胞的增殖、侵袭和迁移有关。

CIP2A, an oncoprotein, is associated with cell proliferation, invasion and migration in laryngeal carcinoma cells.

机构信息

Department of Otolaryngology, First Hospital of Ningbo City, Ningbo City, Zhejiang 315000, P.R. China.

出版信息

Oncol Rep. 2017 Aug;38(2):1005-1012. doi: 10.3892/or.2017.5759. Epub 2017 Jun 27.

DOI:10.3892/or.2017.5759
PMID:28656258
Abstract

Laryngeal carcinoma is one of the most common malignant tumors in otorhinolaryngology. Moreover, experimental investigation showed that cancerous inhibitor of protein phosphatase 2A (CIP2A) expressed highly in various cancers. Therefore, we investigated whether CIP2A can regulate the proliferation, invasion and migration by RNA interference in Hep-2 cells and AMC-NH-8 cells and further affect the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway. Overexpression of CIP2A was evaluated in tumor tissue and laryngeal cancer cell lines (Hep-2 and AMC-NH-8 cells) by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot assay. In a follow-up experiment, we confirmed that CIP2A siRNA effectively suppressed the cell proliferation at 48 and 72 h, and arrested cell cycle at G0/G1 in Hep-2 cells and AMC-NH-8 cells. The invasion and migration of cell in siRNA CIP2A group were markedly inhibited. Moreover, the experimental results showed that the expression levels of invasion- and migration-related genes, including E-cadherin, metastasis-associated gene 1 (MTA1) and matrix metalloproteinases-2/9 (MMP-2/9), were regulated by CIP2A siRNA. Phosphorylation levels of PI3K and AKT proteins were reduced by CIP2A siRNA. Importantly, it suggested signaling through PI3K/Akt as a critical mechanism by which CIP2A siRNA may suppress cell proliferation, invasion and migration in laryngeal carcinoma cells.

摘要

喉癌是耳鼻喉科最常见的恶性肿瘤之一。此外,实验研究表明,蛋白磷酸酶 2A 的致癌抑制剂(CIP2A)在各种癌症中表达水平较高。因此,我们通过 RNA 干扰研究了 CIP2A 是否可以调节 Hep-2 细胞和 AMC-NH-8 细胞的增殖、侵袭和迁移,并进一步影响磷脂酰肌醇 3-激酶(PI3K)/蛋白激酶 B(AKT)通路的激活。通过实时定量聚合酶链反应(RT-qPCR)和 Western blot 检测,评估 CIP2A 在肿瘤组织和喉癌细胞系(Hep-2 和 AMC-NH-8 细胞)中的表达。在后续实验中,我们证实 CIP2A siRNA 可有效抑制 Hep-2 细胞和 AMC-NH-8 细胞在 48 和 72 小时的细胞增殖,并将细胞周期阻滞在 G0/G1 期。siRNA CIP2A 组的细胞侵袭和迁移明显受到抑制。此外,实验结果表明,侵袭和迁移相关基因的表达水平,包括 E-钙黏蛋白、转移相关基因 1(MTA1)和基质金属蛋白酶-2/9(MMP-2/9),受 CIP2A siRNA 调节。CIP2A siRNA 降低了 PI3K 和 AKT 蛋白的磷酸化水平。重要的是,研究表明,PI3K/Akt 信号通路是 CIP2A siRNA 抑制喉癌细胞增殖、侵袭和迁移的关键机制之一。

相似文献

1
CIP2A, an oncoprotein, is associated with cell proliferation, invasion and migration in laryngeal carcinoma cells.CIP2A,一种癌蛋白,与喉癌细胞的增殖、侵袭和迁移有关。
Oncol Rep. 2017 Aug;38(2):1005-1012. doi: 10.3892/or.2017.5759. Epub 2017 Jun 27.
2
Micropeptide CIP2A-BP encoded by LINC00665 inhibits triple-negative breast cancer progression.LINC00665 编码的微肽 CIP2A-BP 抑制三阴性乳腺癌进展。
EMBO J. 2020 Jan 2;39(1):e102190. doi: 10.15252/embj.2019102190. Epub 2019 Nov 22.
3
Overexpression of CIP2A is an independent prognostic indicator in nasopharyngeal carcinoma and its depletion suppresses cell proliferation and tumor growth.CIP2A的过表达是鼻咽癌的一个独立预后指标,其缺失可抑制细胞增殖和肿瘤生长。
Mol Cancer. 2014 May 19;13:111. doi: 10.1186/1476-4598-13-111.
4
Constitutive CHK1 Expression Drives a pSTAT3-CIP2A Circuit that Promotes Glioblastoma Cell Survival and Growth.组成性 CHK1 表达驱动 pSTAT3-CIP2A 回路,促进神经胶质瘤细胞存活和生长。
Mol Cancer Res. 2020 May;18(5):709-722. doi: 10.1158/1541-7786.MCR-19-0934. Epub 2020 Feb 20.
5
Expression and prognostic significance of CIP2A in cutaneous malignant melanoma.CIP2A 在皮肤恶性黑色素瘤中的表达及预后意义。
Biomarkers. 2014 Feb;19(1):70-6. doi: 10.3109/1354750X.2013.871752. Epub 2013 Dec 27.
6
CIP2A down regulation enhances the sensitivity of pancreatic cancer cells to gemcitabine.CIP2A的下调增强了胰腺癌细胞对吉西他滨的敏感性。
Oncotarget. 2016 Mar 22;7(12):14831-40. doi: 10.18632/oncotarget.7447.
7
CIP2A is overexpressed in non-small cell lung cancer and correlates with poor prognosis.CIP2A 在非小细胞肺癌中过表达,并与不良预后相关。
Ann Surg Oncol. 2011 Mar;18(3):857-65. doi: 10.1245/s10434-010-1313-8. Epub 2010 Sep 15.
8
CIP2A is overexpressed in human ovarian cancer and regulates cell proliferation and apoptosis.CIP2A在人类卵巢癌中过度表达,并调节细胞增殖和凋亡。
Tumour Biol. 2012 Dec;33(6):2299-306. doi: 10.1007/s13277-012-0492-2. Epub 2012 Aug 25.
9
Expression of CIP2A in renal cell carcinomas correlates with tumour invasion, metastasis and patients' survival.CIP2A 在肾细胞癌中的表达与肿瘤侵袭、转移和患者生存相关。
Br J Cancer. 2011 Dec 6;105(12):1905-11. doi: 10.1038/bjc.2011.492. Epub 2011 Nov 10.
10
CIP2A is a predictor of poor prognosis in colon cancer.CIP2A 是结直肠癌预后不良的预测因子。
J Gastrointest Surg. 2012 May;16(5):1037-47. doi: 10.1007/s11605-012-1828-3. Epub 2012 Feb 11.

引用本文的文献

1
CIP2A promotes bronchiolitis obliterans by activating the NF‑κB pathway.CIP2A通过激活NF-κB信号通路促进闭塞性细支气管炎。
Mol Med Rep. 2025 Apr;31(4). doi: 10.3892/mmr.2025.13473. Epub 2025 Feb 28.
2
CIP2A interacts with AKT1 to promote the malignant biological behaviors of oral squamous cell carcinoma by upregulating the GSK‑3β/β‑catenin pathway.CIP2A与AKT1相互作用,通过上调GSK‑3β/β‑连环蛋白信号通路来促进口腔鳞状细胞癌的恶性生物学行为。
Exp Ther Med. 2023 Sep 20;26(5):514. doi: 10.3892/etm.2023.12213. eCollection 2023 Nov.
3
High sensitivity CIP2A detection for oral cancer using a rapid transistor-based biosensor module.
使用基于晶体管的快速生物传感器模块对口腔癌进行高灵敏度CIP2A检测。
J Vac Sci Technol B Nanotechnol Microelectron. 2023 Jan;41(1):013201. doi: 10.1116/6.0002175. Epub 2022 Dec 13.
4
CIP2A Promotes Proliferation, Invasion and Chemoresistance to Cisplatin in Renal Cell Carcinoma.CIP2A促进肾细胞癌的增殖、侵袭及对顺铂的化疗耐药性。
J Cancer. 2018 Oct 17;9(21):4029-4038. doi: 10.7150/jca.25005. eCollection 2018.
5
Ascites IL-10 Promotes Ovarian Cancer Cell Migration.腹水白细胞介素-10促进卵巢癌细胞迁移。
Cancer Microenviron. 2018 Dec;11(2-3):115-124. doi: 10.1007/s12307-018-0215-3. Epub 2018 Jul 23.