ArticleOncology letters2021
MicroRNA-186-3p attenuates tumorigenesis of cervical cancer by targeting MCM2.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Proliferative proteome induced by HPV 16E6 and NFX1-123 partnership in longitudinal keratinocyte cultures.Journal of virology · 2025Article
- Article
- Targeting the RUNX3-miR-186-3p-DAT-IGF1R axis as a therapeutic strategy in a Parkinson's disease model.Journal of translational medicine · 2024Article
- Biomedical Promise of Sustainable Microwave-Engineered Symmetric Curcumin Derivatives.Pharmaceutics · 2024Article
- Minichromosome maintenance proteins in lung adenocarcinoma: Clinical significance and therapeutic targets.FEBS open bio · 2023Article
- Application of Protein-Protein Interaction Network Analysis in Order to Identify Cervical Cancer miRNA and mRNA Biomarkers.TheScientificWorldJournal · 2023Article
- MCM2 in human cancer: functions, mechanisms, and clinical significance.Molecular medicine (Cambridge, Mass.) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study examined the effect of microRNA (miRNA/miR)-186-3p and its target gene, minichromosome maintenance complex component 2 (MCM2), on cervical cancer. Cervical cancer tissues and corresponding normal tissues were collected from 48 patients and bioinformatics analysis was performed to identify the differentially expressed genes in cervical cancer. TargetScan and TarBase were used to identify miRNAs, and reverse transcription-quantitative PCR was conducted to detect and evaluate mRNA expression levels. Additionally, MTT and 5-bromo-2-deoxyuridine assays were performed to examine cell proliferation. Cell adhesion, cell cycle distribution and apoptosis were assessed using cell adhesion, flow cytometry and caspase-3/7 activity assays, respectively. The results revealed that miR-186-3p expression was downregulated in cervical cancer tissues and cells, and it negatively regulated MCM2 expression by directly targeting its 3' untranslated region in cervical cancer. Furthermore, MCM2 facilitated cell proliferation and inhibited cell apoptosis, which were reversed by upregulation of miR-186-3p expression. Collectively, the present study suggested that MCM2 and its negative regulator, miR-186-3p, regulate cervical cancer progression.
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Registered trials
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