ArticleHereditas2025
Prognostic value of Linc00662/miR-16-5p/FASN in cervical cancer and regulation of tumor progression.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Therapeutic microRNAs: Mechanisms, Delivery, and Clinical Translation in Oncology.International journal of molecular sciences · 2026Review
- Circular RNAs in cervical cancer: from ceRNA networks to epitranscriptomic regulation, immune modulation, and metastatic reprogramming.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCervical cancer (CC) is the world's single most frequent gynecological cancer, is more than 500,000 new annual cases globally, and is a serious threat to women's reproductive health. LncRNAs have significant effects on human diseases; nevertheless, the expression of Linc00662 in CC and its mechanism of action are not yet entirely clear. The goal of the work was to investigate the expression, prognostic value and biological utility of Linc00662 in CC progression and to identify its underlying mechanisms in molecular terms.
methodsExpression levels of Linc00662, miR-16-5p and FASN in CC tissues and cells were detected through real-time quantitative PCR. Determination of cell proliferative capacity by CCK-8. Cell migration and invasion were assessed through Transwell assay. Binding of Linc00662 to miR-16-5p was mediated through a dual-luciferase reporter gene test was validated.
resultsLinc00662 expression levels were significantly elevated in CC. High Linc00662 expression was strongly linked to increased tumor size, later FIGO staging, poorer tumor differentiation, mesenchymal infiltration, and lymph node metastasis, and high Linc00662 expression predicted a poor prognosis. Silencing Linc00662 reduced the proliferation, migration, and invasion of CC cells. Furthermore, Linc00662 negatively regulated miR-16-5p and indirectly regulated the upregulation of FASN expression.
conclusionsLinc00662 positively regulates FASN expression through targeting miR-16-5p and facilitates CC cell proliferation, migration and invasion, promoting CC progression.
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Registered trials
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