Inhibition of formin like 2 promotes the transition of ectopic endometrial stromal cells to epithelial cells in adenomyosis through a MET-like process
Inhibition of formin like 2 promotes the transition of ectopic endometrial stromal cells to epithelial cells in adenomyosis through a MET-like process
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抑制福尔明样2通过类MET过程促进子宫腺肌症中异位子宫内膜基质细胞向上皮细胞的转变
DOI：
10.1016/j.gene.2019.06.003
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发表时间：
2019-08-20
期刊：
影响因子：
3.5
通讯作者：
Huang, Ouping
中科院分区：
文献类型：
--
作者：
Li, You;Zhang, Quan;Huang, Ouping
EMT（Epithelial-Mesenchymal Transition）是子宫腺肌病发病机制中的重要因素之一。FMNL 2通过促进EMT诱导癌细胞侵袭，但其在子宫腺肌病中的作用尚不清楚。免疫组化染色结果显示，与正常子宫内膜间质细胞相比，子宫腺肌病异位内膜间质细胞中FMNL 2的表达水平明显增高。FMNL 2基因的敲除可抑制异位子宫内膜间质细胞的侵袭和迁移，并促进E-cadherin和Vimentin蛋白的表达。同时，抑制FMNL 2可诱导E-cadherin的细胞膜定位。我们的研究结果表明，FMNL 2的异常激活通过诱导EMT过程促进子宫腺肌病的发病。相反，FMNL 2的抑制促进异位子宫内膜间质细胞通过MET样过程向子宫腺肌病中的上皮细胞转变。
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.