Publication Information

Title m6A mRNA methylation regulates AKT activity to promote the proliferation and tumorigenicity of endometrial cancer
PubMed ID 30154548
Accession GSE93911
Publication Date 2019.05.07
Journal Nature cell biology
Abstract N6-methyladenosine (m6A) messenger RNA methylation is a gene regulatory mechanism affecting cell differentiation and proliferation in development and cancer. To study the roles of m6A mRNA methylation in cell proliferation and tumorigenicity, we investigated human endometrial cancer in which a hotspot R298P mutation is present in a key component of the methyltransferase complex (METTL14). We found that about 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3, another component of the methyltransferase complex. These changes lead to increased proliferation and tumorigenicity of endometrial cancer cells, likely through activation of the AKT pathway. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator mTORC2. Together, these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.

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Regulator Cancer Role Function Upstream Downstream Details

Statistics of dataset in this publication

Statistics of m6A peaks and modified genes

The fold enrichment value of each samples

Top 200 peaks with higher fold enrichment

ChromosomeStartEndGene SymbolStrandFold enrichmentAccession