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为尤因肉瘤构建EWS-FLI1驱动的转基因小鼠模型面临的挑战。

Challenges in modeling EWS-FLI1-driven transgenic mouse model for Ewing sarcoma.

作者信息

Ramachandran Balaji, Rajkumar Thangarajan, Gopisetty Gopal

机构信息

Department of Molecular Oncology, Cancer Institute (W.I.A) No. 38, Sardar Patel Road, Adyar, Chennai 600036, India.

出版信息

Am J Transl Res. 2021 Nov 15;13(11):12181-12194. eCollection 2021.

DOI:
PMID:34956445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8661172/
Abstract

EWS-FLI1 is a master regulator of Ewing sarcoma (ES) oncogenesis. Although EWS-FLI1 represents a clear therapeutic target, targeted therapeutic inhibitors are lacking. Scientific literature has indicated accumulating information pertaining to EWS-FLI1 translocation, pathogenesis, function, oncogenic partnerships, and potential clinical relevance. However, attempts to develop EWS-FLI1-driven human-like ES mouse models or in systems ended up with limited success. Establishing such models as preclinical screening tools may accelerate the development of EWS-FLI1 targeted therapeutic inhibitors. This review summarizes the current scenario, which focuses on the limitations, challenges, and possible reasons for past failures in model development and also plausible alternatives.

摘要

EWS-FLI1是尤因肉瘤（ES）肿瘤发生的主要调节因子。尽管EWS-FLI1是一个明确的治疗靶点，但缺乏靶向治疗抑制剂。科学文献表明，有关EWS-FLI1易位、发病机制、功能、致癌伙伴关系及潜在临床相关性的信息不断积累。然而，尝试开发由EWS-FLI1驱动的类人ES小鼠模型或体外系统，最终取得的成功有限。建立此类模型作为临床前筛选工具可能会加速EWS-FLI1靶向治疗抑制剂的开发。本综述总结了当前的情况，重点关注模型开发中过去失败的局限性、挑战和可能原因，以及合理的替代方案。

相似文献

[1]
Challenges in modeling EWS-FLI1-driven transgenic mouse model for Ewing sarcoma.

Am J Transl Res. 2021-11-15

[2]
High-throughput RNAi screen in Ewing sarcoma cells identifies leucine rich repeats and WD repeat domain containing 1 (LRWD1) as a regulator of EWS-FLI1 driven cell viability.

Gene. 2017-1-5

[3]
Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model.

Oncotarget. 2017-5-23

[4]
BET bromodomain inhibitors suppress EWS-FLI1-dependent transcription and the IGF1 autocrine mechanism in Ewing sarcoma.

Oncotarget. 2016-7-12

[5]
EWS-FLI1 regulates a transcriptional program in cooperation with Foxq1 in mouse Ewing sarcoma.

Cancer Sci. 2018-7-18

[6]
Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis.

J Clin Invest. 2014-12

[7]
SLFN11 Is a Transcriptional Target of EWS-FLI1 and a Determinant of Drug Response in Ewing Sarcoma.

Clin Cancer Res. 2015-9-15

[8]
A novel oncogenic mechanism in Ewing sarcoma involving IGF pathway targeting by EWS/Fli1-regulated microRNAs.

Oncogene. 2011-6-6

[9]
Slit2 signaling stimulates Ewing sarcoma growth.

Genes Cancer. 2022-12-14

[10]
Blocking the road, stopping the engine or killing the driver? Advances in targeting EWS/FLI-1 fusion in Ewing sarcoma as novel therapy.

Expert Opin Ther Targets. 2014-8-27

引用本文的文献

[1]
Ubiquitin-specific protease 6 (USP6) mRNA lipid nanoparticles ignite anti-tumor immunity and suppress tumorigenesis in Ewing sarcoma.

Mol Cancer Ther. 2025-6-25

[2]
Druggable upregulated proteins in EWS-FLI-driven Ewing sarcoma as emerging new therapeutic targets.

Am J Transl Res. 2025-3-15

[3]
YAP1 is a key regulator of EWS::FLI1-dependent malignant transformation upon IGF-1-mediated reprogramming of bone mesenchymal stem cells.

Cell Rep. 2025-3-25

[4]
Refined culture conditions with increased physiological relevance uncover oncogene-dependent metabolic signatures in Ewing sarcoma spheroids.

Cell Rep Methods. 2025-2-24

[5]
Trabectedin promotes oncolytic virus antitumor efficacy, viral gene expression, and immune effector function in models of bone sarcoma.

Mol Ther Oncol. 2024-9-26

[6]
Preclinical models for the study of pediatric solid tumors: focus on bone sarcomas.

Front Oncol. 2024-7-18

[7]
Spontaneous expression of the CIC::DUX4 fusion oncoprotein from a conditional allele potently drives sarcoma formation in genetically engineered mice.

Oncogene. 2024-4

[8]
Expression of the CIC-DUX4 fusion oncoprotein mimics human CIC-rearranged sarcoma in genetically engineered mouse models.

Res Sq. 2023-10-29

[9]
Emerging Pharmacotherapeutic Strategies to Overcome Undruggable Proteins in Cancer.

Int J Biol Sci. 2023

本文引用的文献

[1]
Expression of the EWSR1-FLI1 fusion oncogene in pancreas cells drives pancreatic atrophy and lipomatosis.

Pancreatology. 2020-12

[2]
The local and circulating SOX9 as a potential biomarker for the diagnosis of primary bone cancer.

J Bone Oncol. 2020-5-31

[3]
Wnt/β-catenin-activated Ewing sarcoma cells promote the angiogenic switch.

JCI Insight. 2020-7-9

[4]
Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma.

Nat Commun. 2020-5-15

[5]
Loss of Stag2 cooperates with EWS-FLI1 to transform murine Mesenchymal stem cells.

BMC Cancer. 2020-1-2

[6]
The Fusion Oncogene FUS-CHOP Drives Sarcomagenesis of High-Grade Spindle Cell Sarcomas in Mice.

Sarcoma. 2019-7-25

[7]
CD151 confers metastatic potential to clear cell sarcoma of the soft tissue in animal model.

Oncol Lett. 2019-6

[8]
Anatomic Origin of Osteochondrogenic Progenitors Impacts Sensitivity to EWS-FLI1-Induced Transformation.

Cancers (Basel). 2019-3-6

[9]
Insight into the Etiology of Undifferentiated Soft Tissue Sarcomas from a Novel Mouse Model.

Mol Cancer Res. 2019-1-25

[10]
FusionPathway: Prediction of pathways and therapeutic targets associated with gene fusions in cancer.

PLoS Comput Biol. 2018-7-24

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