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Updated: Feb 25, 2026

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

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Published on: June 27, 2020

LSD1 Performs Demethylase-Independent and Context-Specific Roles in Ewing Sarcoma.

Rachel D Dreher^1,2,3, Cenny Taslim¹, Ira Miller^2,3

¹Center for Childhood Cancer Research, The Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, Ohio.

Cancer Research Communications

|February 24, 2026

Summary

This summary is machine-generated.

Lysine specific demethylase 1 (LSD1) plays a key role in Ewing sarcoma progression by repressing essential genes. Its nonenzymatic functions are crucial, suggesting current therapeutic strategies may be insufficient.

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Published on: November 29, 2016

Area of Science:

Oncology
Molecular Biology
Epigenetics

Background:

Lysine specific demethylase 1 (LSD1) is overexpressed in Ewing sarcoma, correlating with poor prognosis.
LSD1 and EWSR1::FLI1 oncoprotein colocalize, indicating LSD1's role in driving sarcoma progression.
Therapeutic targeting of LSD1 has shown mixed results, with unclear contributions of its enzymatic and nonenzymatic functions.

Purpose of the Study:

To elucidate the enzymatic and nonenzymatic roles of LSD1 in Ewing sarcoma transcriptional regulation.
To identify core genes regulated by LSD1 across multiple Ewing sarcoma cell lines.
To evaluate the effectiveness of current assays in predicting Ewing sarcoma response to LSD1 inhibition.

Main Methods:

Utilized multiple depletion methods across various Ewing sarcoma cell lines.
Performed genome-wide analysis to identify LSD1-regulated genes.
Employed 2D cytotoxicity and proliferation assays, alongside an irreversible inhibitor (OG-L002).

Main Results:

Identified a core set of 22 genes commonly repressed by LSD1, impacting synapse and e-cadherin pathways.
Demonstrated that LSD1 loss leads to early and sustained derepression of these core genes.
Showcased nonenzymatic regulation of e-cadherin target genes, highlighting LSD1's noncanonical roles.
Found that 2D cytotoxicity and proliferation assays may inadequately assess Ewing sarcoma response to LSD1 inhibition.

Conclusions:

LSD1's nonenzymatic activity is critical for Ewing sarcoma progression, particularly in repressing e-cadherin targets.
Understanding both enzymatic and nonenzymatic functions is essential for effective LSD1-targeted therapies.
Current preclinical assays may not fully capture Ewing sarcoma response to LSD1 inhibition, necessitating novel assessment methods.