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Updated: May 14, 2026

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
Published on: June 27, 2020
FOXM1 is an oncogenic mediator in Ewing Sarcoma
Laura Christensen1, Jay Joo, Sean Lee
1Division of Hematology-Oncology, Department of Pediatrics, Saban Research Institute, Childrens Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
FOXM1, a proliferation factor, is expressed in Ewing tumors and drives their growth. Inhibiting FOXM1 with Thiostrepton reduces Ewing tumor cell viability, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Ewing Family Tumors (EFTs) are pediatric bone and soft tissue cancers.
- EFTs are driven by EWS/ETS fusion oncogenes, primarily EWS/FLI1.
- FOXM1 is a proliferation-associated transcription factor implicated in various cancers.
Purpose of the Study:
- To investigate the role of FOXM1 in Ewing tumor pathogenesis.
- To determine if FOXM1 is a downstream target of EWS/FLI1.
- To evaluate the therapeutic potential of FOXM1 inhibition in EFTs.
Main Methods:
- Analysis of FOXM1 expression in Ewing tumor samples and cell lines.
- Assessment of anchorage-independent growth after FOXM1 knockdown.
- Treatment of Ewing cell lines with Thiostrepton, a FOXM1 inhibitor.
- Evaluation of cell viability and apoptosis induction.
Main Results:
- FOXM1 is expressed in Ewing primary tumors and cell lines.
- EWS/FLI1 enhances FOXM1 expression.
- FOXM1 knockdown reduces anchorage-independent growth.
- Thiostrepton treatment decreases FOXM1 expression, reduces cell viability, and induces apoptosis.
Conclusions:
- FOXM1 plays a significant role in Ewing tumor pathogenesis.
- FOXM1 inhibition represents a promising therapeutic strategy for EFTs.
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