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MEDUSA for Identifying Death Regulatory Genes in Chemo-genetic Profiling Data

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Pericentromeric Satellite III transcripts induce etoposide resistance.

Julian Kanne^1,2, Michelle Hussong^1,2, Jörg Isensee³

¹Institute for Translational Epigenetics, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.

Cell Death & Disease

|May 25, 2021

Summary

Long non-coding satellite III RNA (SatIII) confers etoposide resistance in lung cancer by protecting topoisomerase IIa (TOP2A). SatIII expression, influenced by epigenetic modifications, predicts chemotherapy resistance and can be targeted by BRD4 inhibitors.

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Using the E1A Minigene Tool to Study mRNA Splicing Changes

Using the E1A Minigene Tool to Study mRNA Splicing Changes

Published on: April 22, 2021

Area of Science:

Genomics
Molecular Biology
Cancer Research

Background:

Non-coding RNAs from pericentromeric satellite repeats play roles in genome stability and stress responses.
Long non-coding satellite III RNA (SatIII) is induced by heat shock (HS), a condition known to protect against etoposide toxicity.

Purpose of the Study:

To investigate the role of SatIII in etoposide resistance in lung cancer.
To elucidate the mechanism by which SatIII confers resistance.
To explore therapeutic strategies targeting SatIII.

Main Methods:

Analysis of genome methylation profiles in patient-derived xenograft mouse models.
Assessment of SatIII expression under various stress conditions.
Investigation of TOP2A localization and DNA damage in response to etoposide treatment.
Evaluation of BRD4 inhibitors on SatIII expression and etoposide sensitivity.

Main Results:

Epigenetic modification of the SatIII locus and its expression correlate with chemotherapy resistance.
SatIII recruits TOP2A to nuclear stress bodies under stress conditions, protecting it from etoposide.
This recruitment leads to decreased DNA damage upon etoposide treatment.
BRD4 inhibitors reduce SatIII expression, thereby restoring etoposide sensitivity.

Conclusions:

SatIII is a key mediator of etoposide resistance in lung cancer.
SatIII-mediated protection involves the sequestration of TOP2A in nuclear stress bodies.
Targeting SatIII expression with BRD4 inhibitors represents a potential therapeutic strategy to overcome chemotherapy resistance.