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The epitranscriptome meets non-coding RNA: m6A-mediated regulation in oncogenesis and therapy
Prasanna Srinivasan Ramalingam1, Mokhtar Rejili2, Faouzi Haouala2
1Protein Engineering Lab, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
N6-methyladenosine (m6A) modifications are key regulators of RNA metabolism in cancer. Their interplay with non-coding RNAs (ncRNAs) influences tumor progression and drug resistance, offering new therapeutic targets.
Area of Science:
- Epitranscriptomics
- Cancer Biology
- RNA Metabolism
Background:
- N6-methyladenosine (m6A) modifications are crucial epigenetic regulators of RNA processing.
- m6A influences gene expression, impacting oncogenesis, metastasis, and therapeutic resistance.
- The interaction between m6A and non-coding RNAs (ncRNAs) is increasingly recognized in cancer.
Purpose of the Study:
- To review the multifaceted roles of m6A modifications in cancer biology.
- To elucidate the intricate crosstalk between m6A and ncRNAs (miRNAs, lncRNAs, circRNAs).
- To explore the therapeutic potential of targeting ncRNA-m6A interactions in precision oncology.
Main Methods:
- Literature review synthesizing current research on m6A modifications and ncRNAs in cancer.
- Analysis of m6A's impact on RNA stability, translation, and transcript outcomes.
- Examination of reciprocal regulatory mechanisms between m6A machinery and ncRNAs.
Main Results:
- m6A modifications regulate oncogene and tumor suppressor transcripts, promoting cancer hallmarks.
- m6A influences ncRNA biogenesis, stability, and function, creating feedback loops.
- ncRNA-m6A crosstalk impacts the tumor microenvironment, immune response, and drug resistance.
Conclusions:
- The interplay between m6A and ncRNAs is a critical driver of cancer progression and therapeutic resistance.
- Targeting these interactions presents promising avenues for novel cancer therapies.
- Further research is needed to translate these findings into clinical applications for precision oncology.
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