Conclusion
Taken together, these data reveal a differential m6A epitranscriptomic pattern in endometriosis. The N6-methyladenosine modification mediated by METTL3 and METTL14 play a cooperative role in promoting cell proliferation and invasion in a model of endometriosis. Therefore, METTL3 and METTL14 may be a novel treatment target of the disease.
Results
The m6A methylation levels were decreased in 1312 mRNAs and increased in 518 mRNAs; 1797 mRNAs were increased and 2580 mRNAs were reduced in the ectopic endometrium compared with the eutopic endometrium. Pathway analysis found that the genes with hypo-methylated m6A were significantly associated with important pathways in endometriosis, including oestrogen, Hippo, and PI3K-Akt signalling and cell-cell adhesion. Furthermore, METTL3 and METTL14 were downregulated in the ectopic endometrium compared with the eutopic endometrium (P < 0.001). Simultaneous METTL3 and METTL14 knockdown increased cell proliferation and invasion.