• 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

SATB1在癌症进展和转移中的作用:机制与治疗潜力

SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.

作者信息

Bai Jinping, Yang Gege, Yu Qi, Chi Qianya, Zeng Xianlu, Qi Wenjing

机构信息

Department of Bioscience, Changchun Normal University, Changchun, China.

Key Laboratory of Molecular Epigenetics of Ministry of Education, College of Life Sciences, Northeast Normal University, Changchun, China.

出版信息

Front Oncol. 2025 Feb 25;15:1535929. doi: 10.3389/fonc.2025.1535929. eCollection 2025.

DOI:10.3389/fonc.2025.1535929
PMID:40071088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11893431/
Abstract

Cancer remains a major global health challenge, with prostate cancer, lung cancer, colorectal cancer, and breast cancer accounting for nearly half of all diagnoses. Despite advancements in cancer treatment, metastasis to distant organs continues to be the leading cause of cancer-related mortality. The progression of cancer involves the alteration of numerous genes, with dynamic changes in chromatin organization and histone modifications playing a critical role in regulating cancer-associated genes. Special AT-rich sequence-binding protein 1 (SATB1), a critical chromatin organizer, plays a pivotal role in cancer progression by regulating gene expression, chromatin remodeling, and cell signaling pathways. SATB1 binds to AT-rich DNA sequences, acting as a scaffold for chromatin-modifying enzymes and transcription factors, thus coordinating the regulation of extensive gene networks. Its overexpression has been implicated in a wide range of cancers and is associated with poor prognosis, aggressive tumor phenotypes, and enhanced epithelial-mesenchymal transition (EMT). Moreover, SATB1's activity is modulated by microRNAs (miRNAs) and post-translational modifications, further contributing to its complex regulatory functions. Given its crucial involvement in cancer progression and metastasis, SATB1 has emerged as a promising target for novel therapeutic strategies. This review delves into the molecular mechanisms of SATB1 in cancer and explores potential therapeutic approaches for targeting this key regulator in cancer treatment.

摘要

癌症仍然是一项重大的全球健康挑战,前列腺癌、肺癌、结直肠癌和乳腺癌占所有诊断病例的近一半。尽管癌症治疗取得了进展,但远处器官转移仍然是癌症相关死亡的主要原因。癌症的进展涉及众多基因的改变,染色质组织和组蛋白修饰的动态变化在调节癌症相关基因中起着关键作用。特殊富含AT序列结合蛋白1(SATB1)是一种关键的染色质组织者,通过调节基因表达、染色质重塑和细胞信号通路在癌症进展中起关键作用。SATB1与富含AT的DNA序列结合,作为染色质修饰酶和转录因子的支架,从而协调广泛基因网络的调节。其过表达与多种癌症有关,并与预后不良、侵袭性肿瘤表型和上皮-间质转化(EMT)增强有关。此外,SATB1的活性受微小RNA(miRNA)和翻译后修饰的调节,进一步促成其复杂的调节功能。鉴于其在癌症进展和转移中的关键作用,SATB1已成为新型治疗策略的一个有前景的靶点。本综述深入探讨了SATB1在癌症中的分子机制,并探索了在癌症治疗中靶向这一关键调节因子的潜在治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/a7a6647e351f/fonc-15-1535929-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/dcaeb71b0f9e/fonc-15-1535929-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/74ae19bd60ce/fonc-15-1535929-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/e6b94f87d946/fonc-15-1535929-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/0815a58b0c70/fonc-15-1535929-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/a7a6647e351f/fonc-15-1535929-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/dcaeb71b0f9e/fonc-15-1535929-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/74ae19bd60ce/fonc-15-1535929-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/e6b94f87d946/fonc-15-1535929-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/0815a58b0c70/fonc-15-1535929-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff2d/11893431/a7a6647e351f/fonc-15-1535929-g005.jpg

相似文献

1
SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.SATB1在癌症进展和转移中的作用:机制与治疗潜力
Front Oncol. 2025 Feb 25;15:1535929. doi: 10.3389/fonc.2025.1535929. eCollection 2025.
2
Chromatin organizer SATB1 as a novel molecular target for cancer therapy.染色质组织蛋白 SATB1 作为癌症治疗的新型分子靶标。
Curr Drug Targets. 2012 Dec;13(13):1603-15. doi: 10.2174/138945012803530008.
3
The Role of SATB1 in Tumour Progression and Metastasis.SATB1 在肿瘤进展和转移中的作用。
Int J Mol Sci. 2019 Aug 25;20(17):4156. doi: 10.3390/ijms20174156.
4
SATB1 protein is associated with the epithelial‑mesenchymal transition process in non‑small cell lung cancers.SATB1 蛋白与非小细胞肺癌中的上皮-间充质转化过程有关。
Oncol Rep. 2021 Jun;45(6). doi: 10.3892/or.2021.8069. Epub 2021 May 6.
5
SATB1 overexpression regulates the development and progression in bladder cancer through EMT.SATB1过表达通过上皮-间质转化调节膀胱癌的发生发展。
PLoS One. 2015 Feb 23;10(2):e0117518. doi: 10.1371/journal.pone.0117518. eCollection 2015.
6
Loss of special AT-rich binding protein 1 expression is a marker of poor survival in lung cancer.特殊 AT 富含结合蛋白 1 表达缺失是肺癌患者生存预后不良的一个标志。
J Thorac Oncol. 2011 Jul;6(7):1179-89. doi: 10.1097/JTO.0b013e31821b4ce0.
7
Functional relevance of SATB1 in immune regulation and tumorigenesis.SATB1 在免疫调节和肿瘤发生中的功能相关性。
Biomed Pharmacother. 2018 Aug;104:87-93. doi: 10.1016/j.biopha.2018.05.045. Epub 2018 May 14.
8
Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression.Wnt/β-连环蛋白信号传导调控的SATB1促进结直肠癌的肿瘤发生和进展。
Oncogene. 2016 Mar 31;35(13):1679-91. doi: 10.1038/onc.2015.232. Epub 2015 Jul 13.
9
Expression of SATB1 promotes the growth and metastasis of colorectal cancer.SATB1的表达促进结直肠癌的生长和转移。
PLoS One. 2014 Jun 27;9(6):e100413. doi: 10.1371/journal.pone.0100413. eCollection 2014.
10
The Special AT-rich Sequence Binding Protein 1 (SATB1) and its role in solid tumors.特异性富含 AT 的序列结合蛋白 1(SATB1)及其在实体瘤中的作用。
Cancer Lett. 2018 Mar 28;417:96-111. doi: 10.1016/j.canlet.2017.12.031. Epub 2018 Jan 4.

本文引用的文献

1
Triptolide suppresses melanoma cell growth and through the Src-ERK signaling pathway.雷公藤甲素通过Src-ERK信号通路抑制黑色素瘤细胞生长。
J Cancer. 2024 Oct 14;15(19):6345-6354. doi: 10.7150/jca.100840. eCollection 2024.
2
The most recent progress of baicalein in its anti-neoplastic effects and mechanisms.黄芩素在抗肿瘤作用及机制方面的最新进展。
Biomed Pharmacother. 2024 Jul;176:116862. doi: 10.1016/j.biopha.2024.116862. Epub 2024 Jun 7.
3
SATB1, senescence and senescence-related diseases.SATB1、衰老和衰老相关疾病。
J Cell Physiol. 2024 Aug;239(8):e31327. doi: 10.1002/jcp.31327. Epub 2024 May 27.
4
E-cadherin interacts with EGFR resulting in hyper-activation of ERK in multiple models of breast cancer.E-钙黏蛋白与 EGFR 相互作用,导致乳腺癌多种模型中 ERK 的过度激活。
Oncogene. 2024 May;43(19):1445-1462. doi: 10.1038/s41388-024-03007-2. Epub 2024 Mar 20.
5
Loss of p53 epigenetically modulates epithelial to mesenchymal transition in colorectal cancer.p53缺失通过表观遗传调控在结直肠癌中调节上皮-间质转化。
Transl Oncol. 2024 May;43:101848. doi: 10.1016/j.tranon.2023.101848. Epub 2024 Feb 27.
6
SATB1 mediated tumor colonization and β-catenin nuclear localization are associated with colorectal cancer progression.SATB1 介导的肿瘤定植和 β-连环蛋白核定位与结直肠癌的进展相关。
Cancer Biol Ther. 2024 Dec 31;25(1):2320307. doi: 10.1080/15384047.2024.2320307. Epub 2024 Feb 22.
7
Wnt/β-catenin-driven EMT regulation in human cancers.Wnt/β-catenin 驱动的人类癌症中的 EMT 调控。
Cell Mol Life Sci. 2024 Feb 9;81(1):79. doi: 10.1007/s00018-023-05099-7.
8
Triptolide inhibits esophageal squamous cell carcinoma progression by regulating the circNOX4/miR-153-3p/SATB1 signaling pathway.雷公藤红素通过调控 circNOX4/miR-153-3p/SATB1 信号通路抑制食管鳞癌细胞的进展。
Thorac Cancer. 2024 Mar;15(7):538-549. doi: 10.1111/1759-7714.15215. Epub 2024 Jan 24.
9
Depletion of Induces Cell Cycle Arrest in Pancreatic Cancer Cells.耗尽 可诱导胰腺癌细胞周期停滞。
Cancer Genomics Proteomics. 2024 Jan-Feb;21(1):18-29. doi: 10.21873/cgp.20426.
10
Long non-coding RNA LINC00491 accelerates head and neck squamous cell carcinoma progression through regulating miR-508-3p/SATB1 axis and activating Wnt signaling pathway.长链非编码 RNA LINC00491 通过调控 miR-508-3p/SATB1 轴和激活 Wnt 信号通路促进头颈部鳞状细胞癌的进展。
Cytokine. 2024 Mar;175:156444. doi: 10.1016/j.cyto.2023.156444. Epub 2023 Dec 26.