METTL14-mediated RNA methylation in digestive system tumors
International Journal of Molecular Medicine, ISSN: 1791-244X, Vol: 52, Issue: 3
2023
- 5Citations
- 1Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations5
- Citation Indexes5
- Captures1
- Readers1
Article Description
N6-methyladenosine (m6A) RNA methylation is one of the most common post-transcriptional modification mechanism in eukaryotes. m6A is involved in almost all stages of the mRNA life cycle, specifically regulating its stability, splicing, export and translation. Methyltransferase-like 14 (METTL14) is a particularly important m6A methylation 'writer' that can recognize RNA substrates. METTL14 has been documented to improve the activity and catalytic efficiency of METTL3. However, as individual proteins they can also regulate different biological processes. Malignancies in the digestive system are some of the most common malignancies found in humans, which are typically associated with poor prognoses with limited clinical solutions. METTL14-mediated methylation has been implicated in both the potentiation and inhibition of digestive system tumor growth, cell invasion and metastasis, in addition to drug resistance. In the present review, the research progress and regulatory mechanisms of METTL14-mediated methylation in digestive system malignancies were summarized. In addition, future research directions and the potential for its clinical application were examined.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85166528354&origin=inward; http://dx.doi.org/10.3892/ijmm.2023.5289; http://www.ncbi.nlm.nih.gov/pubmed/37539726; http://www.spandidos-publications.com/10.3892/ijmm.2023.5289; https://dx.doi.org/10.3892/ijmm.2023.5289; https://www.spandidos-publications.com/10.3892/ijmm.2023.5289
Spandidos Publications
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