• 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

全面分析急性髓系白血病中10-11易位蛋白（TETs）的表达及预后作用。

Comprehensively analyze the expression and prognostic role for ten-eleven translocations (TETs) in acute myeloid leukemia.

作者信息

Huang Yan, Wei Jie, Huang Xunjun, Zhou Weijie, Xu Yuling, Deng Dong-Hong, Cheng Peng

机构信息

Department of Hematology and Rheumatology, People's Hospital of Baise, Baise, China.

Department of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.

出版信息

Transl Cancer Res. 2020 Nov;9(11):7259-7283. doi: 10.21037/tcr-20-3149.

DOI:10.21037/tcr-20-3149
PMID:35117329
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8798779/
Abstract

BACKGROUND

The ten-eleven translocation (TET) family oxidize 5-methylcytosines (5mCs) and promote the locus-specific reversal of DNA. The role of TETs in acute myeloid leukemia (AML) is mostly unknown.

METHODS

TETs mRNA expression levels were analyzed via Gene Expression Profiling Interactive Analysis (GEPIA). The association TETs expression levels and methylation with prognosis by UALCAN GenomicScape, and METHsurv. We analyzed TETs' aberration types, located mutations, and structures via cBioPortal. GeneMANIA performed the functional network. Gene ontology (GO) enrichment was analyzed via LinkedOmics. MiWalK identified miRNAs, miTarbase, and TargetScan. Transcription factor (TF) targets were analyzed via ChEA3. GSCAlite analyzed the role of these defined genes in cancer pathways and potential drug targets. Finally, we selected AML patients in our department to investigate the mutated types of TETs.

RESULTS

TETs expression level results showed TET1 (P=0.003) and TET2 (P=0.004) overexpressed in Haferlach leukemia samples, TET3 (P=4.04e-8) downregulation in Andersson leukemia samples. TET2 and TET3 overexpression but TET1 downregulation in the GEPIA database. Overexpression of TET2 leads to positive outcomes (P=0.0091). The upregulation of TET2 led to poor survival for CN-AML patients, but downregulation of TET3 indicated a satisfactory prognosis. The hypermethylation of TETs like cg24705708 (P=0.036), cg05976228 (P=0.022), cg19127638 (P=0.022), cg15254238 (P=0.025), cg07669489 (P=0.037) indicate poor outcomes. Overexpression of GALNS (P=0.024) as an adverse biomarker, downregulation of E2F5 (P=0.037), MAP7 (P=0.019), and NRIP1 (P=0.0013) indicated good prognosis. Regulatory network analysis indicated TETs' functions, including covalent chromatin modification, histone modification, DNA methylation, or demethylation. Enrichment functions involving. TETs participate in several cancer pathways, including DNA repair response and receptor tyrosine kinase (RTK) signaling pathway. TETs are sensitive to belinostat, ceranib-2, docetaxel, tivantinib, and vincristine.

CONCLUSION

Present study showed that TETs have different expressions in AML, and the expression levels of TETs lead to different outcomes of AML. The TETs cancer pathway analysis will also provide potential therapy methods for AML patients with TETs aberrations.

摘要

背景

十一-易位（TET）家族可氧化5-甲基胞嘧啶（5mC），并促进位点特异性的DNA去甲基化。TET蛋白在急性髓系白血病（AML）中的作用大多未知。

方法

通过基因表达谱交互分析（GEPIA）分析TET蛋白的mRNA表达水平。利用UALCAN GenomicScape和METHsurv分析TET蛋白表达水平和甲基化与预后的关系。通过cBioPortal分析TET蛋白的畸变类型、定位突变和结构。使用GeneMANIA构建功能网络。通过LinkedOmics进行基因本体（GO）富集分析。利用MiWalK、miTarbase和TargetScan鉴定miRNA。通过ChEA3分析转录因子（TF）靶点。使用GSCAlite分析这些特定基因在癌症通路中的作用及潜在药物靶点。最后，选取本部门的AML患者研究TET蛋白的突变类型。

结果

TET蛋白表达水平结果显示，在Haferlach白血病样本中TET1（P = 0.003）和TET2（P = 0.004）过表达，在Andersson白血病样本中TET3（P = 4.04e - 8）下调。在GEPIA数据库中TET2和TET3过表达但TET1下调。TET2过表达导致阳性结果（P = 0.0091）。TET2上调导致CN - AML患者生存不良，但TET3下调提示预后良好。TET蛋白的高甲基化如cg24705708（P = 0.036）、cg05976228（P = 0.022）、cg19127638（P = 0.022）、cg15254238（P = 0.025）、cg07669489（P = 0.037）提示预后不良。GALNS过表达（P = 0.024）作为不良生物标志物，E2F5（P = 0.037）、MAP7（P = 0.019）和NRIP1（P = 0.0013）下调提示预后良好。调控网络分析表明TET蛋白的功能，包括共价染色质修饰 histone modification、DNA甲基化或去甲基化。富集功能涉及。TET蛋白参与多种癌症通路，包括DNA修复反应和受体酪氨酸激酶（RTK）信号通路。TET蛋白对贝利司他、西拉尼布 - 2、多西他赛、替凡替尼和长春新碱敏感。

结论

本研究表明TET蛋白在AML中表达不同，且TET蛋白的表达水平导致AML的不同预后。TET蛋白的癌症通路分析也将为有TET蛋白畸变的AML患者提供潜在的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/77ff30443198/tcr-09-11-7259-f18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/94162b8997a6/tcr-09-11-7259-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/c628dac62561/tcr-09-11-7259-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/22c755e1d491/tcr-09-11-7259-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/730606344785/tcr-09-11-7259-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/e428fddb7707/tcr-09-11-7259-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/565128ecf8c6/tcr-09-11-7259-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/0d2fb0a71f72/tcr-09-11-7259-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/daac50983419/tcr-09-11-7259-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/5af1bb511bad/tcr-09-11-7259-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/44c88c573dd8/tcr-09-11-7259-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/06cbb5e217e3/tcr-09-11-7259-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/269fb3011818/tcr-09-11-7259-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/ca61e7d21a5d/tcr-09-11-7259-f13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/f271ccf27ada/tcr-09-11-7259-f14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/a29eaf4c127f/tcr-09-11-7259-f15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/aee70bf57c62/tcr-09-11-7259-f16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/acdca580b8ab/tcr-09-11-7259-f17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/77ff30443198/tcr-09-11-7259-f18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/94162b8997a6/tcr-09-11-7259-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/c628dac62561/tcr-09-11-7259-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/22c755e1d491/tcr-09-11-7259-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/730606344785/tcr-09-11-7259-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/e428fddb7707/tcr-09-11-7259-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/565128ecf8c6/tcr-09-11-7259-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/0d2fb0a71f72/tcr-09-11-7259-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/daac50983419/tcr-09-11-7259-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/5af1bb511bad/tcr-09-11-7259-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/44c88c573dd8/tcr-09-11-7259-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/06cbb5e217e3/tcr-09-11-7259-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/269fb3011818/tcr-09-11-7259-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/ca61e7d21a5d/tcr-09-11-7259-f13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/f271ccf27ada/tcr-09-11-7259-f14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/a29eaf4c127f/tcr-09-11-7259-f15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/aee70bf57c62/tcr-09-11-7259-f16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/acdca580b8ab/tcr-09-11-7259-f17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a712/8798779/77ff30443198/tcr-09-11-7259-f18.jpg

相似文献

1
Comprehensively analyze the expression and prognostic role for ten-eleven translocations (TETs) in acute myeloid leukemia.全面分析急性髓系白血病中10-11易位蛋白（TETs）的表达及预后作用。
Transl Cancer Res. 2020 Nov;9(11):7259-7283. doi: 10.21037/tcr-20-3149.
2
Expression and prognosis analysis of family in acute myeloid leukemia.家族在急性髓系白血病中的表达与预后分析。
Aging (Albany NY). 2020 Mar 25;12(6):5031-5047. doi: 10.18632/aging.102928.
3
Analyzing the key gene expression and prognostics values for acute myeloid leukemia.分析急性髓系白血病的关键基因表达及预后价值。
Transl Cancer Res. 2020 Nov;9(11):7284-7298. doi: 10.21037/tcr-20-3177.
4
TET enzymes are successively expressed during human spermatogenesis and their expression level is pivotal for male fertility.TET 酶在人类精子发生过程中依次表达，其表达水平对男性生育能力至关重要。
Hum Reprod. 2016 Jul;31(7):1411-24. doi: 10.1093/humrep/dew096. Epub 2016 May 1.
5
Differential expression of ten-eleven translocation genes in endometrial cancers.子宫内膜癌中10-11易位基因的差异表达
Tumour Biol. 2017 Mar;39(3):1010428317695017. doi: 10.1177/1010428317695017.
6
Identification the prognostic value of glutathione peroxidases expression levels in acute myeloid leukemia.确定谷胱甘肽过氧化物酶表达水平在急性髓系白血病中的预后价值。 （原句中Identification使用错误，应该是Identify）
Ann Transl Med. 2020 Jun;8(11):678. doi: 10.21037/atm-20-3296.
7
miR-93-5p knockdown repressed hepatocellular carcinoma progression via increasing ERBB4 and TETs-dependent DNA demethylation.miR-93-5p 敲低通过增加 ERBB4 和 TETs 依赖性 DNA 去甲基化抑制肝细胞癌进展。
Autoimmunity. 2021 Dec;54(8):547-560. doi: 10.1080/08916934.2021.1969552. Epub 2021 Aug 26.
8
Pan-cancer analysis of oncogenic TNFAIP2 identifying its prognostic value and immunological function in acute myeloid leukemia.泛癌症分析致癌基因 TNFAIP2，鉴定其在急性髓系白血病中的预后价值和免疫功能。
BMC Cancer. 2022 Oct 15;22(1):1068. doi: 10.1186/s12885-022-10155-9.
9
Comprehensive bioinformatic analysis of the expression and prognostic significance of TSC22D domain family genes in adult acute myeloid leukemia.全面的生物信息学分析 TSC22D 结构域家族基因在成人急性髓系白血病中的表达及预后意义。
BMC Med Genomics. 2023 May 27;16(1):117. doi: 10.1186/s12920-023-01550-7.
10
TET (Ten-eleven translocation) family proteins: structure, biological functions and applications.TET（Ten-eleven translocation）家族蛋白：结构、生物学功能及应用。
Signal Transduct Target Ther. 2023 Aug 11;8(1):297. doi: 10.1038/s41392-023-01537-x.

引用本文的文献

1
TET1: The epigenetic architect of clinical disease progression.TET1：临床疾病进展的表观遗传构建者。
Genes Dis. 2025 Jan 4;12(5):101513. doi: 10.1016/j.gendis.2025.101513. eCollection 2025 Sep.
2
5-Hydroxymethylcytosine: Far Beyond the Intermediate of DNA Demethylation.5-羟甲基胞嘧啶：远超 DNA 去甲基化的中间产物。
Int J Mol Sci. 2024 Nov 2;25(21):11780. doi: 10.3390/ijms252111780.
3
Decoding the epitranscriptome: a new frontier for cancer therapy and drug resistance.解析表观转录组：癌症治疗和耐药性的新前沿。

本文引用的文献

1
knockdown inhibits the malignancy progression through downregulating mediated and in acute myeloid leukemia.敲低通过下调介导的作用抑制急性髓系白血病中的恶性进展。
Transl Cancer Res. 2019 Nov;8(7):2526-2534. doi: 10.21037/tcr.2019.10.12.
2
County poverty levels influence genome-wide DNA methylation profiles in African American and European American women.县贫困水平影响非裔美国人和欧裔美国女性的全基因组DNA甲基化谱。
Transl Cancer Res. 2019 Apr;8(2):683-692. doi: 10.21037/tcr.2019.02.07.
3
MAP7 interacts with RC3H1 and cooperatively regulate cell-cycle progression of cervical cancer cells via activating the NF-κB signaling.
Cell Commun Signal. 2024 Oct 21;22(1):513. doi: 10.1186/s12964-024-01854-w.
4
Complete hematologic response after belinostat treatment and allogeneic stem cell transplantation for multiple relapsed/refractory angioimmunoblastic T-cell lymphoma: A case report.贝利司他治疗及异基因干细胞移植后多发性复发/难治性血管免疫母细胞性T细胞淋巴瘤的完全血液学缓解：一例报告
Clin Case Rep. 2023 Jun 23;11(6):e7623. doi: 10.1002/ccr3.7623. eCollection 2023 Jun.
5
Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.造血过程中的表观遗传调控及其在血液系统恶性肿瘤靶向治疗中的意义。
Signal Transduct Target Ther. 2023 Feb 17;8(1):71. doi: 10.1038/s41392-023-01342-6.
6
TAF1 inhibitor Bay-299 induces cell death in acute myeloid leukemia.TAF1抑制剂Bay-299可诱导急性髓系白血病细胞死亡。
Transl Cancer Res. 2021 Dec;10(12):5307-5318. doi: 10.21037/tcr-21-2295.
MAP7 通过激活 NF-κB 信号通路与 RC3H1 相互作用，协同调节宫颈癌细胞的细胞周期进程。
Biochem Biophys Res Commun. 2020 Jun 18;527(1):56-63. doi: 10.1016/j.bbrc.2020.04.008. Epub 2020 Apr 25.
4
MicroRNA-1271-5p inhibits the tumorigenesis of ovarian cancer through targeting E2F5 and negatively regulates the mTOR signaling pathway.微小 RNA-1271-5p 通过靶向 E2F5 抑制卵巢癌的肿瘤发生，并负调控 mTOR 信号通路。
Panminerva Med. 2021 Sep;63(3):336-342. doi: 10.23736/S0031-0808.20.03939-7. Epub 2020 May 14.
5
E2F5 promotes prostate cancer cell migration and invasion through regulation of TFPI2, MMP-2 and MMP-9.E2F5 通过调节 TFPI2、MMP-2 和 MMP-9 促进前列腺癌细胞迁移和侵袭。
Carcinogenesis. 2020 Dec 31;41(12):1767-1780. doi: 10.1093/carcin/bgaa043.
6
MAP7 promotes migration and invasion and progression of human cervical cancer through modulating the autophagy.微管相关蛋白7通过调节自噬促进人宫颈癌的迁移、侵袭及进展。
Cancer Cell Int. 2020 Jan 13;20:17. doi: 10.1186/s12935-020-1095-4. eCollection 2020.
7
Cancer statistics, 2020.癌症统计数据，2020 年。
CA Cancer J Clin. 2020 Jan;70(1):7-30. doi: 10.3322/caac.21590. Epub 2020 Jan 8.
8
The growing landscape of FLT3 inhibition in AML.AML 中不断发展的 FLT3 抑制治疗领域。
Hematology Am Soc Hematol Educ Program. 2019 Dec 6;2019(1):539-547. doi: 10.1182/hematology.2019000058.
9
Hypoxia-induced autophagy drives colorectal cancer initiation and progression by activating the PRKC/PKC-EZR (ezrin) pathway.缺氧诱导的自噬通过激活 PRKC/PKC-EZR（埃兹蛋白）通路促进结直肠癌的发生和发展。
Autophagy. 2020 Aug;16(8):1436-1452. doi: 10.1080/15548627.2019.1687213. Epub 2019 Nov 27.
10
CDK2 suppression synergizes with all-trans-retinoic acid to overcome the myeloid differentiation blockade of AML cells.CDK2 抑制与全反式维甲酸协同作用，克服 AML 细胞的髓系分化阻断。
Pharmacol Res. 2020 Jan;151:104545. doi: 10.1016/j.phrs.2019.104545. Epub 2019 Nov 15.