RETRACTED ARTICLE: miR-96-5p regulated TGF-β/SMAD signaling pathway and suppressed endometrial cell viability and migration via targeting TGFBR1

Silei Chen, Yajuan Luo, Liangyi Cui, Qing Yang
Cell cycle (Georgetown, Tex.) · 2020 · vol. 19(14) , pp. 1740–1753 · doi:10.1080/15384101.2020.1777804 · PMID:32635855 · W3036734714
article OA: bronze CC0 RETRACTED ⤵ 13 in-corpus citations
Retraction notice. Marked retracted by OpenAlex; see publisher for the formal retraction notice.
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study found that miR-96-5p, downregulated in endometriosis, suppresses endometrial cell viability and migration by targeting TGFBR1 and inhibiting the TGF-β/SMAD signaling pathway.

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Abstract

We previously performed high throughput RNA-seq in paired eutopic and ectopic endometrial specimen of endometriosis patients, and validated the results by qRT-PCR in endometriosis endometrial tissues. MiR-96-5p was significantly downregulated in ectopic endometrial tissues compared to eutopic tissues. In order to identify the role of miR-96-5p in endometriosis and endometrial cells, and investigate the underlying mechanisms, the Ishikawa and End1/E6E7 cell lines were transfected with miR-96-5p mimics, miR-96-5p inhibitors or TGFBR1 siRNA. The expression of TGF-β/SMAD signaling pathway components and epithelial-mesenchymal transition (EMT) markers were examined by qRT-PCR and western blot, and cell viability and migration were determined by CCK-8, transwell and wound healing assays, respectively. We discovered miR-96-5p to be significantly downregulated while TGFBR1 was distinctly up-regulated in endometriosis. Overexpression of miR-96-5p inhibited endometrial cells viability and migration, while inhibition of miR-96-5p had opposite effect. Furthermore, we confirmed TGFBR1 was a direct target of miR-96-5p. Overexpression of miR-96-5p could block the TGF-β/SMAD signaling pathway via targeting TGFBR1 and reverse the TGF-β1 induced EMT in endometrial cell lines. In conclusion, we demonstrated that miR-96-5p interacted with TGF-β/SMAD signaling pathway and blocked the TGF-β1 induced EMT in endometrial cells via directly targeting TGFBR1.

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Condition tags

endometriosis

MeSH descriptors

Cell Movement Endometrium MicroRNAs Receptor, Transforming Growth Factor-beta Type I Signal Transduction Smad Proteins Transforming Growth Factor beta1 Adult Base Sequence Cell Movement Cell Survival Cell Survival Choristoma Choristoma Down-Regulation Down-Regulation Endometrium Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Female

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References (32)

Cited by (13)

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europepmc
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openalex
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