• 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

KLF17 转录调控转移 [Id] 特性。

Transcriptional regulation of metastatic [Id]entity by KLF17.

机构信息

Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.

出版信息

Genome Biol. 2009;10(11):244. doi: 10.1186/gb-2009-10-11-244. Epub 2009 Nov 30.

DOI:10.1186/gb-2009-10-11-244
PMID:19951400
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3091312/
Abstract

A novel in vivo screening approach has identified KLF17 as a key metastasis suppressor gene that acts through regulation of Id1 transcription factor-dependent induction of the epithelial-to-mesenchymal transition.

摘要

一种新的体内筛选方法鉴定出 KLF17 是一种关键的转移抑制基因，它通过调节 Id1 转录因子依赖性诱导上皮-间充质转化来发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba7/3091312/2ea683a9aa29/gb-2009-10-11-244-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba7/3091312/2ea683a9aa29/gb-2009-10-11-244-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba7/3091312/2ea683a9aa29/gb-2009-10-11-244-1.jpg

相似文献

1
Transcriptional regulation of metastatic [Id]entity by KLF17.KLF17 转录调控转移 [Id] 特性。
Genome Biol. 2009;10(11):244. doi: 10.1186/gb-2009-10-11-244. Epub 2009 Nov 30.
2
KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer.KLF17是乳腺癌上皮-间质转化和转移的负调控因子。
Nat Cell Biol. 2009 Nov;11(11):1297-304. doi: 10.1038/ncb1974. Epub 2009 Oct 4.
3
Tumor-suppressive p53 Signaling Empowers Metastatic Inhibitor KLF17-dependent Transcription to Overcome Tumorigenesis in Non-small Cell Lung Cancer.肿瘤抑制性p53信号增强转移性抑制剂KLF17依赖性转录以克服非小细胞肺癌中的肿瘤发生。
J Biol Chem. 2015 Aug 28;290(35):21336-51. doi: 10.1074/jbc.M114.635730. Epub 2015 Apr 24.
4
Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.Krüppel样因子17，一种新型肿瘤抑制因子：其低表达与癌症转移有关。
Tumour Biol. 2016 Feb;37(2):1505-13. doi: 10.1007/s13277-015-4588-3. Epub 2015 Dec 12.
5
Identification of a novel inhibitor of differentiation-1 (ID-1) binding partner, caveolin-1, and its role in epithelial-mesenchymal transition and resistance to apoptosis in prostate cancer cells.一种新型分化抑制因子-1（ID-1）结合蛋白小窝蛋白-1的鉴定及其在前列腺癌细胞上皮-间质转化和抗凋亡中的作用
J Biol Chem. 2007 Nov 16;282(46):33284-33294. doi: 10.1074/jbc.M705089200. Epub 2007 Sep 12.
6
Gain-of-function of mutant p53: mutant p53 enhances cancer progression by inhibiting KLF17 expression in invasive breast carcinoma cells.突变型p53的功能获得：突变型p53通过抑制浸润性乳腺癌细胞中的KLF17表达来促进癌症进展。
Cancer Lett. 2014 Nov 1;354(1):87-96. doi: 10.1016/j.canlet.2014.07.045. Epub 2014 Aug 8.
7
2-Hydroxycinnamaldehyde inhibits the epithelial-mesenchymal transition in breast cancer cells.2-羟基肉桂醛抑制乳腺癌细胞的上皮-间充质转化。
Breast Cancer Res Treat. 2013 Feb;137(3):697-708. doi: 10.1007/s10549-012-2388-7. Epub 2013 Jan 3.
8
Architectural transcription factor HMGI(Y) promotes tumor progression and mesenchymal transition of human epithelial cells.结构转录因子HMGI(Y)促进人类上皮细胞的肿瘤进展和间充质转化。
Mol Cell Biol. 2001 Jan;21(2):575-94. doi: 10.1128/MCB.21.2.575-594.2001.
9
Epithelial-mesenchymal transition and the invasive potential of tumors.上皮-间质转化与肿瘤的侵袭潜能
Trends Mol Med. 2008 May;14(5):199-209. doi: 10.1016/j.molmed.2008.03.004. Epub 2008 Apr 10.
10
Suppressed Krüppel‑like factor 17 expression induces tumor proliferation, metastasis and a poor prognosis in papillary thyroid carcinoma.Krüppel样因子17表达受抑制会诱导甲状腺乳头状癌的肿瘤增殖、转移并导致预后不良。
Mol Med Rep. 2014 Oct;10(4):2087-92. doi: 10.3892/mmr.2014.2429. Epub 2014 Jul 29.

引用本文的文献

1
The causal relationship between immune cells and diabetic retinopathy: a Mendelian randomization study.免疫细胞与糖尿病视网膜病变的因果关系：一项孟德尔随机化研究。
Front Immunol. 2024 Sep 2;15:1381002. doi: 10.3389/fimmu.2024.1381002. eCollection 2024.
2
The Upstream 1350~1250 Nucleotide Sequences of the Human Gene Contain Critical -Elements Responsible for Upregulating Its Transcription during ER Stress.人类基因的上游 1350~1250 个核苷酸序列包含关键元件，这些元件负责在 ER 应激期间上调其转录。
Int J Mol Sci. 2023 Dec 12;24(24):17393. doi: 10.3390/ijms242417393.
3
The Role and Research Progress of Inhibitor of Differentiation 1 in Atherosclerosis.

本文引用的文献

1
KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer.KLF17是乳腺癌上皮-间质转化和转移的负调控因子。
Nat Cell Biol. 2009 Nov;11(11):1297-304. doi: 10.1038/ncb1974. Epub 2009 Oct 4.
2
p53 controls cancer cell invasion by inducing the MDM2-mediated degradation of Slug.p53通过诱导MDM2介导的Slug降解来控制癌细胞的侵袭。
Nat Cell Biol. 2009 Jun;11(6):694-704. doi: 10.1038/ncb1875. Epub 2009 May 17.
3
The HIF-1-active microenvironment: an environmental target for cancer therapy.
分化抑制因子 1 在动脉粥样硬化中的作用及研究进展。
DNA Cell Biol. 2022 Feb;41(2):71-79. doi: 10.1089/dna.2021.0745. Epub 2022 Jan 19.
4
Genotypes and Phenotypes: A Search for Influential Genes in Diabetic Retinopathy.基因型与表型：探寻糖尿病视网膜病变中的相关基因
Int J Mol Sci. 2020 Apr 14;21(8):2712. doi: 10.3390/ijms21082712.
5
Do Genomic Factors Play a Role in Diabetic Retinopathy?基因组因素在糖尿病视网膜病变中起作用吗？
J Clin Med. 2020 Jan 14;9(1):216. doi: 10.3390/jcm9010216.
6
Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.Krüppel样因子17，一种新型肿瘤抑制因子：其低表达与癌症转移有关。
Tumour Biol. 2016 Feb;37(2):1505-13. doi: 10.1007/s13277-015-4588-3. Epub 2015 Dec 12.
7
Low expression of KLF17 is associated with tumor invasion in esophageal carcinoma.KLF17低表达与食管癌的肿瘤侵袭相关。
Int J Clin Exp Pathol. 2015 Sep 1;8(9):11157-63. eCollection 2015.
8
Tumor-suppressive p53 Signaling Empowers Metastatic Inhibitor KLF17-dependent Transcription to Overcome Tumorigenesis in Non-small Cell Lung Cancer.肿瘤抑制性p53信号增强转移性抑制剂KLF17依赖性转录以克服非小细胞肺癌中的肿瘤发生。
J Biol Chem. 2015 Aug 28;290(35):21336-51. doi: 10.1074/jbc.M114.635730. Epub 2015 Apr 24.
9
KLF17 empowers TGF-β/Smad signaling by targeting Smad3-dependent pathway to suppress tumor growth and metastasis during cancer progression.KLF17通过靶向Smad3依赖性途径增强TGF-β/Smad信号传导，从而在癌症进展过程中抑制肿瘤生长和转移。
Cell Death Dis. 2015 Mar 12;6(3):e1681. doi: 10.1038/cddis.2015.48.
10
Proteomic profile and in silico analysis in metastatic melanoma with and without BRAF mutation.有BRAF突变和无BRAF突变的转移性黑色素瘤的蛋白质组学特征及计算机模拟分析
PLoS One. 2014 Dec 1;9(12):e112025. doi: 10.1371/journal.pone.0112025. eCollection 2014.
缺氧诱导因子-1激活的微环境：癌症治疗的一个环境靶点。
Adv Drug Deliv Rev. 2009 Jul 2;61(7-8):623-32. doi: 10.1016/j.addr.2009.01.006. Epub 2009 May 3.
4
Metastasis: from dissemination to organ-specific colonization.转移：从播散到器官特异性定植。
Nat Rev Cancer. 2009 Apr;9(4):274-84. doi: 10.1038/nrc2622.
5
Sp1 phosphorylation and its regulation of gene transcription.Sp1磷酸化及其对基因转录的调控。
Mol Cell Biol. 2009 May;29(10):2483-8. doi: 10.1128/MCB.01828-08. Epub 2009 Mar 9.
6
Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits.上皮细胞与间充质细胞状态之间的转变：恶性特征和干细胞特征的获得。
Nat Rev Cancer. 2009 Apr;9(4):265-73. doi: 10.1038/nrc2620. Epub 2009 Mar 5.
7
Learning therapeutic lessons from metastasis suppressor proteins.从转移抑制蛋白中汲取治疗经验。
Nat Rev Cancer. 2009 Apr;9(4):253-64. doi: 10.1038/nrc2594. Epub 2009 Feb 26.
8
The epithelial-mesenchymal transition generates cells with properties of stem cells.上皮-间质转化产生具有干细胞特性的细胞。
Cell. 2008 May 16;133(4):704-15. doi: 10.1016/j.cell.2008.03.027.
9
Mechanisms of malignant progression.恶性进展机制。
Carcinogenesis. 2008 Jun;29(6):1092-5. doi: 10.1093/carcin/bgn104. Epub 2008 May 2.
10
Angiotensin II-inducible platelet-derived growth factor-D transcription requires specific Ser/Thr residues in the second zinc finger region of Sp1.血管紧张素II诱导的血小板衍生生长因子-D转录需要Sp1第二个锌指区域中的特定丝氨酸/苏氨酸残基。
Circ Res. 2008 Feb 29;102(4):e38-51. doi: 10.1161/CIRCRESAHA.107.167395. Epub 2008 Feb 7.