ArticleBioengineered2021
MicroRNA miR-106a-5p targets forkhead box transcription factor FOXC1 to suppress the cell proliferation, migration, and invasion of ectopic endometrial stromal cells via the PI3K/Akt/mTOR signaling pathway.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Spatial transcriptomics uncovers the hybrid molecular identity, ciliated phenotype, and immune signature of adenomyosis lesions.Science advances · 2026Article
- Kisspeptins inhibit ectopic endometrial cell invasion and angiogenesis by suppressing PI3K/AKT signaling pathway via CREB5 in endometriosis.International journal of medical sciences · 2026Article
- Mechanism of FOXC1 in the invasion and migration of ectopic endometrial stromal cells in endometriosis.Pflugers Archiv : European journal of physiology · 2025Article
- Obesity as a Catalyst for Endometrial Hyperplasia and Cancer Progression: A Narrative Review of Epidemiology, Molecular Pathways, and Prevention.Biomedicines · 2025Review
- Upregulation of miR-183 inhibits the invasion and migration of endometrial stromal cells in endometriosis patients by downregulating Ezrin.Frontiers in oncology · 2025Article
- Evidence for KISS-1 nuclear translocation and PI3K/AKT signaling in the ultrastructurally and morphometrically analyzed human endometriosis.Frontiers in cell and developmental biology · 2025Article
- mTOR inhibitors as potential therapeutics for endometriosis: a narrative review.Molecular human reproduction · 2024Review
- Focusing on the role of protein kinase mTOR in endometrial physiology and pathology: insights for therapeutic interventions.Molecular biology reports · 2024Review
- IGF2BP2 regulates the proliferation and migration of endometrial stromal cells through the PI3K/AKT/mTOR signaling pathway in Hu sheep.Journal of animal science · 2024Article
- Signatures of necroptosis-related genes as diagnostic markers of endometriosis and their correlation with immune infiltration.BMC women's health · 2023Article
- Endometriosis-Associated Ovarian Carcinomas: How PI3K/AKT/mTOR Pathway Affects Their Pathogenesis.Biomolecules · 2023Review
- The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022Review
- Circular RNA hsa_circ_0011324 is involved in endometrial cancer progression and the evolution of its mechanism.Bioengineered · 2022Article
- Article
- MicroRNA and Alternative mRNA Splicing Events in Cancer Drug Response/Resistance: Potent Therapeutic Targets.Biomedicines · 2021Review
- miR-186-3p attenuates the tumorigenesis of cervical cancer via targeting insulin-like growth factor 1 to suppress PI3K-Akt signaling pathway.Bioengineered · 2021Article
- Long non-coding RNA VCAN-AS1 promotes the malignant behaviors of breast cancer by regulating the miR-106a-5p-mediated STAT3/HIF-1α pathway.Bioengineered · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has exhibited an obvious decreased expression of miR-106a-5p in the ectopic endometrial tissue of endometriosis (EMS) patients. Thus far, the pathophysiological function of miR-106a-5p in EMS is unknown. A previous study showed an increased FOXC1 expression in the ectopic endometrial tissue of patients with EMS. Moreover, we found that there was a binding site of miR-106a-5p on the 3'UTR of FOXC1 through bioinformatics predictions. Hence, we speculated that miR-106a-5p might affect the development of EMS via targeting FOXC1. We first showed a decreased level of miR-106a-5p and an increased level of FOXC1 mRNA in ectopic endometrial tissues compared with normal tissues. Functionally, we transfected ectopic endometrial stromal cells (ESCs) with miR-106a-5p mimics or NC mimics and indicated an inhibitory role of miR-106a-5p on ESC proliferation, invasion, and migration. Mechanistically, FOXC1 was found to be a target gene of miR-106a-5p. To confirm whether miR-106a-5p exerted an inhibitory activity in ESCs via targeting FOXC1, miR-106a-5p mimic was co-transfected into ESCs with the FOXC1-plasmid or vector. We found that FOXC1 overexpression evidently reversed the results caused by a miR-106a-5p mimic in ESCs. Additionally, our results demonstrated that miR-106a-5p mimic inhibited the expression of p-Akt and p-PI3K. Collectively, these results revealed that miR-106a-5p inhibited the proliferative, migratory, and invasive ability of ESCs via directly binding to FOXC1, likely through the suppression of the PI3K and its downstream signaling pathway, which offered a potential and novel therapeutic strategy for EMS treatment.
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