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Updated: Jan 8, 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 at Nationwide Children's Hospital, Columbus, OH, 43215, USA.

Biorxiv : the Preprint Server for Biology

|December 19, 2025

Summary

This summary is machine-generated.

Lysine specific demethylase 1 (LSD1) plays a key role in Ewing sarcoma progression. This study reveals both enzymatic and nonenzymatic functions of LSD1, impacting gene repression and suggesting new therapeutic strategies.

Keywords:

Ewing sarcoma LSD1 OG-L002 UM171 nonenzymatic functions transcriptomics

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Published on: November 29, 2016

Area of Science:

Oncology
Molecular Biology
Epigenetics

Background:

Lysine specific demethylase 1 (LSD1), encoded by KDM1A, is overexpressed in Ewing sarcoma, correlating with poor prognosis.
LSD1 and the EWSR1::FLI1 oncoprotein interact genome-wide, implicating LSD1 in Ewing sarcoma progression.
Previous therapeutic targeting of LSD1 yielded mixed results, with unclear mechanisms of action.

Purpose of the Study:

To elucidate the enzymatic and nonenzymatic roles of LSD1 in Ewing sarcoma transcriptional regulation.
To identify specific genes regulated by LSD1 in Ewing sarcoma.
To evaluate the efficacy of LSD1 inhibition strategies beyond standard cytotoxicity assays.

Main Methods:

Utilized multiple depletion methods across various Ewing sarcoma cell lines.
Performed genome-wide analysis to identify LSD1-regulated genes.
Employed enzymatic and nonenzymatic LSD1 activity assays.
Investigated drug response using 2D cytotoxicity and proliferation assays with an irreversible inhibitor (OG-L002).

Main Results:

Identified a core set of 22 genes commonly repressed by LSD1, impacting synapse function and e-cadherin.
Observed derepression of these genes upon LSD1 loss, consistent across all tested cell lines.
Differentiated gene sets regulated by enzymatic versus nonenzymatic LSD1 activity.
Found repression of e-cadherin target genes to be mediated by nonenzymatic LSD1 activity.
Demonstrated that standard 2D assays may be insufficient for assessing Ewing sarcoma response to LSD1 inhibition.

Conclusions:

LSD1 exerts both enzymatic and nonenzymatic functions in Ewing sarcoma, contributing to disease progression.
Nonenzymatic roles of LSD1, such as regulating e-cadherin, are crucial and represent potential therapeutic targets.
Standard cytotoxicity assays may not accurately reflect therapeutic responses to LSD1 inhibitors in Ewing sarcoma.
Further investigation into the noncanonical functions of chromatin regulatory enzymes is warranted.