ArticleIn vitro cellular & developmental biology. Animal2015
Upregulation of miR-197 inhibits cell proliferation by directly targeting IGFBP5 in human uterine leiomyoma cells.
Article in In vitro cellular & developmental biology. Animal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- miR-335-5p Inhibits Progression of Uterine Leiomyoma by Targeting ARGLU1.Computational and mathematical methods in medicine · 2022Article
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- The Role of miRNA and Related Pathways in Pathophysiology of Uterine Fibroids-From Bench to Bedside.International journal of molecular sciences · 2020Review
- MicroRNA Dysregulation in Pulmonary Arteries from Chronic Obstructive Pulmonary Disease. Relationships with Vascular Remodeling.American journal of respiratory cell and molecular biology · 2018Article
- miR-197 is downregulated in cervical carcinogenesis and suppresses cell proliferation and invasion through targeting forkhead box M1.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uterine leiomyoma (ULM), one of the most common reproductive tract neoplasms in premenopausal women, is a kind of benign tumor with multigene involved. Finding and studying the key gene involved has been a long-needed factor for developing non-surgery therapy and prevention methods. The dysregulated microRNAs were reported to play important roles in ULM pathobiology by regulating tumor growth. Our investigations have revealed that miR-197 is at low expression in ULM. Characterization of the effects of miR-197 in ULM demonstrated that downregulation of miR-197 increased cell growth and induced cell cycle arrest in the G0/G1 phase in vitro, while upregulation of miR-197 expression had the opposite effect on ULM growth and progression. Further research on the mechanism of miR-197 on the proliferation of ULM cells, we showed that miR-197 inhibited cell proliferation of ULM by directly targeting IGFBP5, which was overexpressed in ULM and played an important role in the etiology of ULM. These findings obtained in this study deliver insights and further expand our understanding of the role of miR-197 and its target IGFBP5 in ULM development, which provides a potential novel therapeutic agent to target the proliferation of ULM cells.
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