Abstract
Recently, N6-methyl-adenosine (m6A) ribonucleic acid (RNA) modification, a critical and common internal RNA modification in higher eukaryotes, has generated considerable research interests. Extensive studies have revealed that non-coding RNA m6A modifications (e.g. microRNAs, long non-coding RNAs, and circular RNAs) are associated with tumorigenesis, metastasis, and other tumour characteristics; in addition, they are crucial molecular regulators of cancer progression. In this review, we discuss the relationship between non-coding RNA m6A modification and cancer progression from the perspective of various cancers. In particular, we focus on important mechanisms in tumour progression such as proliferation, apoptosis, invasion and metastasis, tumour angiogenesis. In addition, we introduce clinical applications to illustrate more vividly that non-coding RNA m6A modification has broad research prospects. With this review, we aim to summarize the latest insights and ideas into non-coding RNA m6A modification in cancer progression and targeted therapy, facilitating further research.
Highlights
In eukaryotic cells, some non-coding ribonucleic acids, such as microRNAs, long non-coding RNAs, and circular RNAs, usually do not encode proteins but perform their respective biological functions at the RNA level
The miR-107/LAST2 axis is regulated by the m6A “eraser” ALKBH5 in an HuR-dependent manner to decrease YAP activity and inhibit tumour growth (Jin et al, 2020); long non-coding ribonucleic acid (lncRNA) MALAT1 is stabilized by the METTL3/YTHDF1 complex and its RNA level is increased with high levels of m6A modification (Jin et al, 2019)
Unlike enhancing downstream target mRNA stability, METTL3 has been reported to combine with the m6A “reader” YTHDF2 to promote the degradation of PTEN mRNA and increase tumour malignancy, and subtly, the oncogenic lncRNA LINC00470 serves as an accelerator in this process (Yan et al, 2020)
Summary
Some non-coding ribonucleic acids (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), usually do not encode proteins but perform their respective biological functions at the RNA level. The decrease of endonuclease Dicer leads to aberrant miRNA expression, and modulates the binding of m6A-related enzymes to mRNAs that contain miRNA binding sites, downregulating the abundance of m6A modification without affecting the expression of m6A regulators, METTL3, FTO, and ALKBH5 (Chen et al, 2015). Several studies have enriched our understanding of the interactions between ncRNA and m6A modification, and indicated that aberrant expression of m6A regulators and m6A modification on ncRNAs can alter normal biological processes This abnormal biological change caused by m6A modification makes ncRNAs involved in tumorigenesis and cancer progression, associating with cell proliferation and apoptosis, invasion and metastasis, cell stemness, drug resistance and other mechanisms that enhance the malignancy of cells and the difficulty of cancer therapies. We aim to summarize the latest insights into ncRNA m6A modification in cancer progression and targeted therapy, facilitating further research
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