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LncRNA EPR-induced METTL7A1 modulates target gene translation
Paola Briata1, Luca Caputo2, Ettore Zapparoli3
1Gene Expression Regulation Laboratory, IRCCS Ospedale Policlinico San Martino, 16132 Genova, Italy.
Nucleic Acids Research
|June 24, 2022
Summary
EPR lncRNA targets Mettl7a1 to control mammary cell proliferation. METTL7A1 protein, a target of EPR, regulates translation and suppresses breast cancer cell transformation.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Long non-coding RNAs (lncRNAs) play crucial roles in gene regulation.
- EPR is a lncRNA that controls mammary gland cell proliferation.
- Understanding lncRNA targets is vital for cancer research.
Purpose of the Study:
- To identify direct targets of EPR.
- To elucidate the mechanism by which EPR regulates its targets.
- To investigate the role of EPR targets in mammary gland development and breast cancer.
Main Methods:
- Chromatin interaction analysis to study 3D genome organization.
- Gene expression analysis (mRNA and protein levels).
- Cell proliferation and transformation assays.
- Subcellular localization and protein interaction studies.
Main Results:
- Mettl7a1 is identified as a direct transcriptional target of EPR.
- EPR induces Mettl7a1 transcription by altering chromatin interactions.
- METTL7A1 inhibits TGF-β signaling and attenuates mammary tumor cell transformation.
- METTL7A1's methyltransferase activity is not required for its tumor-suppressive function.
- METTL7A1 localizes to the cytoplasm, interacts with translation machinery, and regulates protein levels post-transcriptionally.
Conclusions:
- EPR regulates Mettl7a1 transcription, impacting mammary cell proliferation and TGF-β signaling.
- METTL7A1 functions as a tumor suppressor in breast cancer by modulating mRNA translation.
- METTL7A1 represents a potential therapeutic target for breast cancer treatment.
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