Down-regulation of circ_0061140 attenuates ectopic endometrial cell proliferation, migration and invasion in endometriosis via inactivating Notch2

Anchun Xu, Xu A, Jiang M, Mengxi Jiang, Li S, Shanshan Li, Qunkao Fei, Fei Q
Gene · 2020 · vol. 757 , pp. 144926 · doi:10.1016/j.gene.2020.144926 · PMID:32621951 · W3039009900
article OA: closed CC0 ⤵ 9 in-corpus citations
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This study investigated the role of circ_0061140 in endometriosis, finding that its down-regulation inhibits ectopic endometrial cell proliferation, migration, and invasion by inactivating the Notch2 pathway.

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Abstract

Endometriosis is a frequent gynecologic disease in the world. CircRNAs can exert a crucial role in various diseases. Nevertheless, little is known about its roles in endometriosis. We investigated the involvement of circ_0061140 in endometriosis. Tissues from endometriosis women displayed an increased expression of circ_0061140. Then, we found loss of circ_0061140 significantly repressed ectopic endometrial cell proliferation, migration and invasion. Meanwhile,miR-140-3pcan demonstrate an important role in several cancers.Here, we reported miR-140-3p was reduced in ectopic endometrial cells and it acted as a target of circ_0061140. Moreover, miR-140-3p was able to reverse the effect of circ_0061140 on ectopic endometrial cells. Furthermore, Notch2 was predicted as a putative target of miR-140-3p. A positive correlation between circ_0061140 and Notch2 was indicated. miR-140-3p and Notch2 were operated as downstream effectors in the circ_0061140 mediated signaling in endometriosis. Decrease of circ_0061140 could depress endometriosis progression through modulating miR-140-3p and Notch2.

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Condition tags

endometriosis

MeSH descriptors

Cell Movement Cell Proliferation Endometriosis RNA, Circular Cells, Cultured Down-Regulation Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans MicroRNAs MicroRNAs MicroRNAs Receptor, Notch2 Receptor, Notch2 Receptor, Notch2

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