ArticleOpen medicine (Warsaw, Poland)2019
microRNA-27a-3p Down-regulation Inhibits Malignant Biological Behaviors of Ovarian Cancer by Targeting BTG1.
Article in Open medicine (Warsaw, Poland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular mechanism ofTranslational cancer research · 2026Article
- Expression patterns of plasma microRNAs in patients with cervical cancer from two teaching hospitals in Ghana.Journal of cancer research and clinical oncology · 2025Article
- Robust Identification of Differential Gene Expression Patterns from Multiple Transcriptomics Datasets for Early Diagnosis, Prognosis, and Therapies for Breast Cancer.Medicina (Kaunas, Lithuania) · 2023Article
- Deregulated miRNA clusters in ovarian cancer: Imperative implications in personalized medicine.Genes & diseases · 2022Review
- The roles ofFrontiers in genetics · 2022Article
- The genetic and epigenetic regulation ofFrontiers in immunology · 2022Article
- miR‑27a‑3p regulates the inhibitory influence of endothelin 3 on the tumorigenesis of papillary thyroid cancer cells.Molecular medicine reports · 2021Article
- Overexpression of miR-27a predicts poor prognosis and promotes the progression in cholangiocarcinoma.Clinical and experimental medicine · 2021Article
- FBLN5 is targeted by microRNA‑27a‑3p and suppresses tumorigenesis and progression in high‑grade serous ovarian carcinoma.Oncology reports · 2020Article
- BTG1 Overexpression Might Promote Invasion and Metastasis of Colorectal CancerFrontiers in oncology · 2020Article
- MiR-27a-3p Regulated the Aggressive Phenotypes of Cervical Cancer by Targeting FBXW7.Cancer management and research · 2020Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Ovarian cancer is the most deadly malignant tumor. MicroRNA-27a-3p (miR-27a-3p) was a tumor oncogene in various cancers. However, the role and mechanism of miR-27a-3p in ovarian cancer are still unknown. In this study, we found that miR-27a-3p over-expression could significantly promote the viability of SK-OV-3 cells, enhance cell migration and invasion, and reduce cell apoptosis. Besides, results from western blot assay showed that miR-27a-3p over-expression could increase Bcl-2 protein expression and decrease Bax protein expression. Furthermore, TargetScan and the dual luciferase reporter gene assay revealed that BTG anti-proliferation factor 1 (BTG1) was a direct target of miR-27a-3p. In addition, we found that miR-27a-3p down-regulation suppressed SK-OV-3 cell viability, migration and invasion, and promoted cell apoptosis. All the effects of miR-27a-3p down-regulation on SK-OV-3 cells were reversed by BTG1-siRNA. Therefore, miR-27a-3p/BTG1 axis may be a new potential target for the treatment of ovarian cancer.
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