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探索上皮-间质转录因子在血液系统恶性肿瘤和实体瘤中的作用:一项系统综述

Exploring the Role of Epithelial-Mesenchymal Transcriptional Factors Involved in Hematological Malignancy and Solid Tumors: A Systematic Review.

作者信息

Kanwal Rimsha, Esposito Jessica Elisabetta, Jawed Bilal, Zakir Syed Khuram, Pulcini Riccardo, Martinotti Riccardo, Botteghi Matteo, Gaudio Francesco, Martinotti Stefano, Toniato Elena

机构信息

Centre of Advanced Studies and Technology, Department of Innovative Technology in Medicine and Dentistry, G.d' Annunzio University, 66100 Chieti, Italy.

Unit of Clinical Pathology and Microbiology, Miulli Generale Hospital, 70021 Acquaviva delle Fonti, Italy.

出版信息

Cancers (Basel). 2025 Feb 5;17(3):529. doi: 10.3390/cancers17030529.

DOI:10.3390/cancers17030529
PMID:39941895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11817253/
Abstract

BACKGROUND

The epithelial mesenchymal transition (EMT) is a biological process in which epithelial cells lose their polarity and adhesion characteristics, and adopt a mesenchymal phenotype. While the EMT naturally occurs during tissue fibrosis, wound healing, and embryonic development, it can be exploited by cancer cells and is strongly associated with cancer stem cell formation, tissue invasiveness, apoptosis, and therapy resistance. Transcription factors (TFs) such as SNAIL, ZEB, and TWIST play a pivotal role in driving the EMT. This systematic review aims to assess the impact of EMT-TFs on hematological malignancy and solid tumors.

METHODS

English-language literature published between 2010 and 2024 was systematically reviewed, utilizing databases such as PubMed and Google Scholar.

RESULTS

A total of 3250 studies were extracted. Of these, 92 publications meeting the inclusion criteria were analyzed to elucidate the role of EMT-TFs in cancer. The results demonstrated that the EMT-TFs play a critical role in both hematological and solid tumor development and progression. They promote invasive, migratory, and metastatic properties in these tumors, and contribute to therapeutic challenges by enhancing chemoresistance. A strong correlation between EMT-TFs and poor overall survival has been identified.

CONCLUSIONS

Our research concluded that EMT-TFs may serve as important predictive and prognostic factors, as well as potential therapeutic targets to mitigate cancer progression.

摘要

背景

上皮-间质转化(EMT)是一个生物学过程,在此过程中上皮细胞失去其极性和黏附特性,并呈现间质表型。虽然EMT自然发生于组织纤维化、伤口愈合和胚胎发育过程中,但癌细胞也可利用这一过程,并且它与癌症干细胞形成、组织侵袭性、细胞凋亡及治疗耐药性密切相关。SNAIL、ZEB和TWIST等转录因子(TFs)在驱动EMT过程中起关键作用。本系统评价旨在评估EMT-TFs对血液系统恶性肿瘤和实体瘤的影响。

方法

系统检索2010年至2024年间发表的英文文献,利用PubMed和谷歌学术等数据库。

结果

共提取3250项研究。其中,对92篇符合纳入标准的出版物进行分析,以阐明EMT-TFs在癌症中的作用。结果表明,EMT-TFs在血液系统恶性肿瘤和实体瘤的发生发展中均起关键作用。它们促进这些肿瘤的侵袭、迁移和转移特性,并通过增强化疗耐药性带来治疗挑战。已确定EMT-TFs与总体生存率差之间存在密切关联。

结论

我们的研究得出结论,EMT-TFs可能作为重要的预测和预后因素,以及减轻癌症进展的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/726532f30750/cancers-17-00529-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/df2b8752afbd/cancers-17-00529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/1ec80224443f/cancers-17-00529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/a9e4a3a728d8/cancers-17-00529-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/726532f30750/cancers-17-00529-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/df2b8752afbd/cancers-17-00529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/1ec80224443f/cancers-17-00529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/a9e4a3a728d8/cancers-17-00529-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3091/11817253/726532f30750/cancers-17-00529-g004.jpg

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[Interpretation on the report of global cancer statistics 2022].[《2022年全球癌症统计报告》解读]
Zhonghua Zhong Liu Za Zhi. 2024 Jul 23;46(7):710-721. doi: 10.3760/cma.j.cn112152-20240416-00152.
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ZEB1 shapes AML immunological niches, suppressing CD8 T cell activity while fostering Th17 cell expansion.ZEB1 塑造 AML 免疫生态位,抑制 CD8 T 细胞活性,同时促进 Th17 细胞扩增。
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IL-17A Promotes the Migration, Invasion and the EMT Process of Lung Cancer Accompanied by NLRP3 Activation.
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IL-17A 促进 NLRP3 激活伴肺癌的迁移、侵袭和 EMT 过程。
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MACC1 promotes pancreatic cancer metastasis by interacting with the EMT regulator SNAI1.MACC1 通过与 EMT 调节因子 SNAI1 相互作用促进胰腺癌转移。
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Bone marrow overexpression of SNAI1 is an early indicator of intrinsic drug resistance in patients with de novo acute myeloid leukemia.SNAI1在骨髓中的过表达是初发急性髓系白血病患者内在耐药性的早期指标。
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Novel Insights on Lipid Metabolism Alterations in Drug Resistance in Cancer.癌症耐药中脂质代谢改变的新见解
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RNA demethylase ALKBH5 inhibits TGF-β-induced EMT by regulating TGF-β/SMAD signaling in non-small cell lung cancer.RNA 去甲基酶 ALKBH5 通过调节非小细胞肺癌中的 TGF-β/SMAD 信号通路抑制 TGF-β 诱导的 EMT。
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PROX1 promotes breast cancer invasion and metastasis through WNT/β-catenin pathway via interacting with hnRNPK.PROX1 通过与 hnRNPK 相互作用,通过 WNT/β-catenin 通路促进乳腺癌的侵袭和转移。
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