ArticleBMC cancer2025
miR-101-3p represses the migratory and invasive abilities of ovarian cancer cells.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- LncRNA DLGAP1-AS2 promotes ESCC progression and indicates unfavorable prognosis via the miR-101-3p/EZH2 axis.Discover oncology · 2026Article
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Authors and funding
7 authors.
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Abstract
backgroundThe study aimed to assess the effects of miR-101-3p on the migratory and invasive abilities of ovarian cancer cells, specifically in the SKOV3 and OVCAR-3 cell lines.
methodsThe expression of miR-101-3p was overexpressed in SKOV3 and OVCAR-3 ovarian cancer cell lines via mimic transfection. The effects on cell viability, migration, and invasion were evaluated using CCK8, wound healing, and Transwell assays, respectively. RNA sequencing was subsequently performed to identify differentially expressed genes.
resultsOverexpression of miR-101-3p significantly decreased cell viability, migration, and invasion in both SKOV3 and OVCAR-3 cells. Transcriptomic analysis identified numerous differentially expressed genes, including FN-1 and CXCL8. Intriguingly, while miR-101-3p suppressed FN-1 mRNA in SKOV3 cells, it led to an increase in both FN-1 and CXCL8 mRNA levels in OVCAR-3 cells, despite inhibiting their invasive phenotype.
conclusionsOur study confirms that miR-101-3p acts as a tumor suppressor in ovarian cancer. The paradoxical regulation of downstream gene transcripts highlights a complex, cell-type-specific regulatory network. This suggests that the overall phenotypic effect of miR-101-3p is an integrated outcome of modulating multiple targets, rather than a linear pathway, and underscores its potential as a therapeutic target requiring further mechanistic study. CLINICAL TRIAL NUMBER: Not applicable.
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