Inhibition of formin like 2 promotes the transition of ectopic endometrial stromal cells to epithelial cells in adenomyosis through a MET-like process

You Li, Li Y, Quan Zhang, Zhang Q, Liu F, Faying Liu, Ziyu Zhang, Zhang Z, Yang Zou, Zou Y, Bicheng Yang, Yang B, Yong Luo, Luo Y, Wang L, Liqun Wang, Ouping Huang, Huang O
Gene · 2019 · vol. 710 , pp. 186–192 · doi:10.1016/j.gene.2019.06.003 · PMID:31175924 · W2950393572
article OA: closed CC0 ⤵ 7 in-corpus citations
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This study investigated how inhibiting formin like 2 impacts ectopic endometrial stromal cells in adenomyosis, finding it promotes their transition into epithelial cells via a MET-like process.

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Abstract

EMT (Epithelial-Mesenchymal Transition) is one of the factors in the pathogenesis of adenomyosis. FMNL2 induced invasion of cancer cell through promoting EMT, but it is unclear the role of FMNL2 in the adenomyosis. By IHC staining, we found the expression level of FMNL2 was significantly higher in the ectopic endometrial stromal cells from women with adenomyosis when compared with normal endometrial stromal cells. Knockdown of FMNL2 inhibited the invasion and migration of ectopic endometrial stromal cells and promoted the protein levels of E-cadherin and Vimentin. Meanwhile, inhibition of FMNL2 could induce the cell membrane localization of E-cadherin. Our findings reveal that the aberrant activation of FMNL2 promotes the pathogenesis of adenomyosis through inducing the EMT process. On the contrary, inhibition of FMNL2 promotes the transition of ectopic endometrial stromal cells to epithelial cells in adenomyosis through a MET-like process.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Epithelial Cells Proteins Stromal Cells Up-Regulation Adenomyosis Adenomyosis Adult Antigens, CD Antigens, CD Cadherins Cadherins Cell Movement Cell Proliferation Cells, Cultured Epithelial Cells Epithelial Cells Epithelial-Mesenchymal Transition Female Formins

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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.

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