Inhibition of METTL3/m6A/miR126 promotes the migration and invasion of endometrial stromal cells in endometriosis

Li X, Xiaoou Li, Wenqian Xiong, Xiong W, Xuefeng Long, Long X, Dai X, Xin Dai, Peng Y, Yuan Peng, Peng Yuan, Xu Y, Ying Xu, Zhang Z, Zhibing Zhang, Ling Zhang, Zhang L, Yi Liu, Liu Y
Biology of reproduction · 2021 · vol. 105(5) , pp. 1221–1233 · doi:10.1093/biolre/ioab152 · PMID:34382070 · PMC10308507 · W3188216863
article OA: green CC0 ⤵ 32 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

METTL3 downregulation reduces m6A levels in endometriosis, promoting endometrial stromal cell migration and invasion via the METTL3/m6A/miR126 pathway.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

N 6-methyladenosine (m6A), one of the most abundant RNA modifications, is involved in the progression of many diseases, but its role and related molecular mechanisms in endometriosis remain unknown. To address these issues, we detected m6A levels in normal, eutopic, and ectopic endometrium and found the m6A levels decreased in eutopic and ectopic endometrium compared with normal endometrium. In addition, we proved that methyltransferase-like 3 (METTL3) downregulation accounted for m6A reduction in endometriosis. Furthermore, we observed that METTL3 knockdown facilitated the migration and invasion of human endometrial stromal cells (HESCs), whereas METTL3 overexpression exerted opposite effects, suggesting that METTL3 downregulation might contribute to endometriosis development by enhancing cellular migration and invasion. Mechanistically, METTL3-dependent m6A was involved in the DGCR8-mediated maturation of primary microRNA126 (miR126 and pri-miR126). Moreover, miR126 inhibitor significantly enhanced the migration and invasion of METTL3-overexpressing HESCs, whereas miR126 mimics attenuated the migration and invasion of METTL3-silenced HESCs. Our study revealed the METTL3/m6A/miR126 pathway, whose inhibition might contribute to endometriosis development by enhancing cellular migration and invasion. It also showed that METTL3 might be a novel diagnostic biomarker and therapeutic target for endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Movement Endometriosis Epithelial Cells Methyltransferases MicroRNAs Stromal Cells Cell Movement Down-Regulation Endometriosis Endometrium Endometrium Epithelial Cells Female Humans Methyltransferases Methyltransferases MicroRNAs MicroRNAs Stromal Cells

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (85)

Cited by (32)

Source provenance

europepmc
last seen: 2026-08-25T06:10:03.373225+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:24:26.422845+00:00
License: CC0 · commercial use OK