• 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

相似文献

1
Oncogenic AURKA-enhanced N-methyladenosine modification increases DROSHA mRNA stability to transactivate STC1 in breast cancer stem-like cells.致癌 AURKA 增强的 N-甲基腺苷修饰增加了 DROSHA mRNA 的稳定性，从而在乳腺癌干细胞样细胞中转激活 STC1。
Cell Res. 2021 Mar;31(3):345-361. doi: 10.1038/s41422-020-00397-2. Epub 2020 Aug 28.
2
FOXM1 recruits nuclear Aurora kinase A to participate in a positive feedback loop essential for the self-renewal of breast cancer stem cells.叉头框蛋白M1招募细胞核极光激酶A以参与乳腺癌干细胞自我更新所必需的正反馈循环。
Oncogene. 2017 Jun 15;36(24):3428-3440. doi: 10.1038/onc.2016.490. Epub 2017 Jan 23.
3
Nuclear AURKA acquires kinase-independent transactivating function to enhance breast cancer stem cell phenotype.细胞核AURKA获得非激酶依赖性反式激活功能以增强乳腺癌干细胞表型。
Nat Commun. 2016 Jan 19;7:10180. doi: 10.1038/ncomms10180.
4
SIX3, a tumor suppressor, inhibits astrocytoma tumorigenesis by transcriptional repression of AURKA/B.SIX3，一种肿瘤抑制因子，通过转录抑制 AURKA/B 来抑制星形细胞瘤的发生。
J Hematol Oncol. 2017 Jun 8;10(1):115. doi: 10.1186/s13045-017-0483-2.
5
Hypoxia-inducible factors regulate pluripotency factor expression by ZNF217- and ALKBH5-mediated modulation of RNA methylation in breast cancer cells.缺氧诱导因子通过ZNF217和ALKBH5介导的乳腺癌细胞RNA甲基化调节来调控多能性因子表达。
Oncotarget. 2016 Oct 4;7(40):64527-64542. doi: 10.18632/oncotarget.11743.
6
The mitotic kinase Aurora--a promotes distant metastases by inducing epithelial-to-mesenchymal transition in ERα(+) breast cancer cells.有丝分裂激酶 Aurora-A 通过诱导 ERα(+)乳腺癌细胞发生上皮-间充质转化促进远处转移。
Oncogene. 2014 Jan 30;33(5):599-610. doi: 10.1038/onc.2012.628. Epub 2013 Jan 21.
7
The PIN1-YTHDF1 axis promotes breast tumorigenesis via the mA-dependent stabilization of AURKA mRNA.PIN1-YTHDF1 轴通过 mA 依赖性稳定 AURKA mRNA 促进乳腺癌发生。
Arch Pharm Res. 2024 Jan;47(1):66-81. doi: 10.1007/s12272-023-01480-z. Epub 2023 Dec 26.
8
A novel Lnc408 maintains breast cancer stem cell stemness by recruiting SP3 to suppress CBY1 transcription and increasing nuclear β-catenin levels.一种新型长链非编码 RNA Lnc408 通过招募 SP3 抑制 CBY1 转录并增加核 β-连环蛋白水平来维持乳腺癌干细胞干性。
Cell Death Dis. 2021 May 1;12(5):437. doi: 10.1038/s41419-021-03708-6.
9
Drosha-independent miR-6778-5p strengthens gastric cancer stem cell stemness via regulation of cytosolic one-carbon folate metabolism.无 Drosha 依赖的 miR-6778-5p 通过调节细胞质一碳叶酸代谢来增强胃癌干细胞干性。
Cancer Lett. 2020 May 28;478:8-21. doi: 10.1016/j.canlet.2020.02.040. Epub 2020 Mar 4.
10
p62/SQSTM1 enhances breast cancer stem-like properties by stabilizing MYC mRNA.p62/SQSTM1通过稳定MYC信使核糖核酸增强乳腺癌干细胞样特性。
Oncogene. 2017 Jan 19;36(3):304-317. doi: 10.1038/onc.2016.202. Epub 2016 Jun 27.

引用本文的文献

1
RNA mA modification: a key regulator in normal and malignant processes.RNA mA修饰：正常和恶性过程中的关键调节因子。
Cell Investig. 2025 Jun;1(2). doi: 10.1016/j.clnves.2025.100023. Epub 2025 Jun 6.
2
Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.将表观遗传调节因子作为克服癌症治疗耐药性的一条有前景的途径。
Signal Transduct Target Ther. 2025 Jul 18;10(1):219. doi: 10.1038/s41392-025-02266-z.
3
N6-methyladenosine-modified GPX2 impacts cancer cell stemness and TKI resistance through regulating of redox metabolism.N6-甲基腺苷修饰的GPX2通过调节氧化还原代谢影响癌细胞干性和对酪氨酸激酶抑制剂的耐药性。
Cell Death Dis. 2025 Jun 18;16(1):458. doi: 10.1038/s41419-025-07764-0.
4
Summary of the mechanism of ferroptosis regulated by m6A modification in cancer progression.m6A修饰调控癌症进展中细胞铁死亡的机制综述。
Front Cell Dev Biol. 2025 Apr 9;13:1507171. doi: 10.3389/fcell.2025.1507171. eCollection 2025.
5
IMPlications of IMP2 in RNA Biology and Disease.IMP2在RNA生物学和疾病中的影响。
Int J Mol Sci. 2025 Mar 7;26(6):2415. doi: 10.3390/ijms26062415.
6
[Characteristics of Aurora Kinase A-Mediated Tumor Microenvironment in Colorectal Cancer and Mining of Active Compounds From Chinese Herbs].[极光激酶A介导的结直肠癌肿瘤微环境特征及中药活性成分挖掘]
Sichuan Da Xue Xue Bao Yi Xue Ban. 2025 Jan 20;56(1):59-67. doi: 10.12182/20250160104.
7
Targeting "don't eat me" signal: breast cancer immunotherapy.靶向“别吃我”信号：乳腺癌免疫疗法
Breast Cancer Res Treat. 2025 Jun;211(2):277-292. doi: 10.1007/s10549-025-07659-w. Epub 2025 Mar 18.
8
Gut dysbiosis conveys psychological stress to activate LRP5/β-catenin pathway promoting cancer stemness.肠道菌群失调传递心理压力以激活LRP5/β-连环蛋白通路，促进癌症干性。
Signal Transduct Target Ther. 2025 Mar 5;10(1):79. doi: 10.1038/s41392-025-02159-1.
9
A novel photoelectrochemical strategy for ultrasensitive and simultaneous detection of 5-methylcytosine and N6-methyladenosine based on proximity binding-triggered assembly MNAzyme -mediated HRCA.一种基于邻近结合触发组装的MNAzyme介导的HRCA用于超灵敏同时检测5-甲基胞嘧啶和N6-甲基腺苷的新型光电化学策略。
Mikrochim Acta. 2025 Feb 26;192(3):192. doi: 10.1007/s00604-025-07033-z.
10
Aurora A Kinase Inhibition Is Synthetic Lethal With the Activation of MYCN in Retinoblastoma.极光激酶A抑制与视网膜母细胞瘤中MYCN激活具有合成致死性。
Invest Ophthalmol Vis Sci. 2025 Feb 3;66(2):20. doi: 10.1167/iovs.66.2.20.

本文引用的文献

1
Clinical and Therapeutic Implications of Cancer Stem Cells.癌症干细胞的临床与治疗意义
N Engl J Med. 2019 Jun 6;380(23):2237-2245. doi: 10.1056/NEJMra1804280.
2
Where, When, and How: Context-Dependent Functions of RNA Methylation Writers, Readers, and Erasers.在哪里、何时以及如何：RNA 甲基化写入器、读取器和擦除器的上下文相关功能。
Mol Cell. 2019 May 16;74(4):640-650. doi: 10.1016/j.molcel.2019.04.025.
3
Stress-induced epinephrine enhances lactate dehydrogenase A and promotes breast cancer stem-like cells.应激诱导的肾上腺素增强乳酸脱氢酶 A 并促进乳腺癌干细胞样细胞。
J Clin Invest. 2019 Mar 1;129(3):1030-1046. doi: 10.1172/JCI121685. Epub 2019 Jan 28.
4
The Biology of mA RNA Methylation in Normal and Malignant Hematopoiesis.mRNA 甲基化在正常和恶性造血中的生物学。
Cancer Discov. 2019 Jan;9(1):25-33. doi: 10.1158/2159-8290.CD-18-0959. Epub 2018 Dec 21.
5
-Methyladenosine modification: a novel pharmacological target for anti-cancer drug development.N6-甲基腺苷修饰：抗癌药物研发的新型药理学靶点。
Acta Pharm Sin B. 2018 Oct;8(6):833-843. doi: 10.1016/j.apsb.2018.06.001. Epub 2018 Jun 6.
6
mA mRNA methylation regulates AKT activity to promote the proliferation and tumorigenicity of endometrial cancer.mA mRNA 甲基化调节 AKT 活性，促进子宫内膜癌的增殖和致瘤性。
Nat Cell Biol. 2018 Sep;20(9):1074-1083. doi: 10.1038/s41556-018-0174-4. Epub 2018 Aug 27.
7
De Novo Molecular Design of a Novel Octapeptide That Inhibits In Vivo Melanogenesis and Has Great Transdermal Ability.新型八肽的从头分子设计，抑制体内黑色素生成，具有很强的透皮能力。
J Med Chem. 2018 Aug 9;61(15):6846-6857. doi: 10.1021/acs.jmedchem.8b00737. Epub 2018 Jul 27.
8
Dynamic transcriptomic mA decoration: writers, erasers, readers and functions in RNA metabolism.动态转录组 mA 修饰：RNA 代谢中的写入器、擦除器、读取器及其功能。
Cell Res. 2018 Jun;28(6):616-624. doi: 10.1038/s41422-018-0040-8. Epub 2018 May 22.
9
SWISS-MODEL: homology modelling of protein structures and complexes.SWISS-MODEL：蛋白质结构和复合物的同源建模。
Nucleic Acids Res. 2018 Jul 2;46(W1):W296-W303. doi: 10.1093/nar/gky427.
10
SUMOylation of the m6A-RNA methyltransferase METTL3 modulates its function.SUMOylation 修饰 m6A 甲基转移酶 METTL3 调节其功能。
Nucleic Acids Res. 2018 Jun 1;46(10):5195-5208. doi: 10.1093/nar/gky156.

致癌 AURKA 增强的 N-甲基腺苷修饰增加了 DROSHA mRNA 的稳定性，从而在乳腺癌干细胞样细胞中转激活 STC1。

Oncogenic AURKA-enhanced N-methyladenosine modification increases DROSHA mRNA stability to transactivate STC1 in breast cancer stem-like cells.

机构信息

Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, China.

State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Guangzhou, Guangdong, 510060, China.

出版信息

Cell Res. 2021 Mar;31(3):345-361. doi: 10.1038/s41422-020-00397-2. Epub 2020 Aug 28.

DOI:10.1038/s41422-020-00397-2
PMID:32859993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8027457/
Abstract

RNase III DROSHA is upregulated in multiple cancers and contributes to tumor progression by hitherto unclear mechanisms. Here, we demonstrate that DROSHA interacts with β-Catenin to transactivate STC1 in an RNA cleavage-independent manner, contributing to breast cancer stem-like cell (BCSC) properties. DROSHA mRNA stability is enhanced by N-methyladenosine (mA) modification which is activated by AURKA in BCSCs. AURKA stabilizes METTL14 by inhibiting its ubiquitylation and degradation to promote DROSHA mRNA methylation. Moreover, binding of AURKA to DROSHA transcript further strengthens the binding of the mA reader IGF2BP2 to stabilize mA-modified DROSHA. In addition, wild-type DROSHA, but not an mA methylation-deficient mutant, enhances BCSC stemness maintenance, while inhibition of DROSHA mA modification attenuates BCSC traits. Our study unveils the AURKA-induced oncogenic mA modification as a key regulator of DROSHA in breast cancer and identifies a novel DROSHA transcriptional function in promoting the BCSC phenotype.

摘要

RNase III DROSHA 在多种癌症中上调，并通过迄今尚不清楚的机制促进肿瘤进展。在这里，我们证明 DROSHA 与 β-Catenin 相互作用以非 RNA 切割依赖性方式激活 STC1，有助于乳腺癌干细胞样细胞 (BCSC) 的特性。DROSHA mRNA 的稳定性通过 N-甲基腺苷 (mA) 修饰增强，mA 修饰在 BCSC 中被 AURKA 激活。AURKA 通过抑制 METTL14 的泛素化和降解来稳定 METTL14，从而促进 DROSHA mRNA 甲基化。此外，AURKA 与 DROSHA 转录本的结合进一步增强了 mA 读蛋白 IGF2BP2 与稳定 mA 修饰的 DROSHA 的结合。此外，野生型 DROSHA，但不是 mA 甲基化缺陷突变体，增强了 BCSC 干性维持，而抑制 DROSHA mA 修饰则减弱了 BCSC 特征。我们的研究揭示了 AURKA 诱导的致癌 mA 修饰作为乳腺癌中 DROSHA 的关键调节剂，并确定了 DROSHA 在促进 BCSC 表型中的新转录功能。