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The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage
Orit Feldstein, Tal Nizri, Tirza Doniger
1The Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan 52900, Israel. doron.ginsberg@biu.ac.il.
Molecular Cancer
|October 31, 2013
Summary
A novel long non-coding RNA, ERIC, is regulated by E2F transcription factors and restricts apoptosis. ERIC acts in a negative feedback loop with E2F1, modulating cell death following DNA damage.
Area of Science:
- Molecular Biology
- Gene Regulation
Background:
- Thousands of long non-coding RNAs (lncRNAs) regulate gene expression and cell fate.
- Transcriptional regulation of lncRNAs is not fully understood.
- E2F1, a key transcription factor, regulates proliferation and cell death and is often deregulated in tumors due to retinoblastoma pathway inactivation.
Purpose of the Study:
- To investigate the transcriptional regulation of lncRNAs.
- To identify novel lncRNAs regulated by E2F transcription factors.
- To elucidate the role of a novel lncRNA, ERIC, in E2F1-mediated apoptosis and DNA damage response.
Main Methods:
- Analysis of ERIC expression upon E2F1/E2F3 activation.
- Knockdown experiments for E2F1/E2F3 to assess ERIC levels.
- Chromatin immunoprecipitation to confirm E2F1 binding to the ERIC promoter.
- Cell cycle analysis and apoptosis assays.
- Assessment of ERIC expression and function following DNA damage induced by Etoposide.
Main Results:
- ERIC (XLOC 006942) is identified as a novel lncRNA regulated by E2F1 and E2F3.
- ERIC expression is cell cycle-dependent, peaking in G1, and is controlled by E2F1.
- Endogenous E2F1 binds to the ERIC promoter.
- Inhibition of ERIC enhances E2F1-induced apoptosis and apoptosis following DNA damage.
- ERIC levels increase upon DNA damage.
Conclusions:
- ERIC is a novel lncRNA transcriptionally regulated by E2Fs.
- ERIC acts as a negative feedback regulator, restricting E2F1-mediated apoptosis.
- ERIC plays a role in the cellular response to DNA damage, modulating apoptosis.
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