ArticleOncoTargets and therapy2020
High Expression of miR-196b Predicts Poor Prognosis in Patients with Ovarian Cancer.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Research progress on the interaction between intestinal flora and microRNA in pelvic inflammatory diseases.Non-coding RNA research · 2025Review
- Utilization of miRNAs as Biomarkers for the Diagnosis, Prognosis, and Metastasis in Gynecological Malignancies.International journal of molecular sciences · 2024Review
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsTo analyze the clinical significance of miR-196b expression in ovarian cancer and predict the function and possible mechanism of miR-196b.
methodsBoth Kaplan-Meier (K-M) and Cox proportional hazards regression model were used to analyze the prognostic factors of patients with ovarian cancer. MiR196-b was modulated in ovarian cancer cells, and the cell viability, cell cycle, and cell cycle-related gene expression were analyzed. The target genes of miR-196b were then predicted and checked the relationship between the target genes.
resultsMiR-196b was an independent risk factor, while high expression of miR-196b was associated with poor prognosis of ovarian cancer. MiR-196b overexpression increased cancer cell proliferation. Cdkn1b, as one of the targets of miR-196b, was related to cell viability and mitosis.
conclusionHigh expression of miR-196b was significantly associated with poor prognosis of the patients with ovarian cancer. MiR-196b could increase the cell proliferation of ovarian cancer by modulating Cdkn1b expression.
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