ArticleScientific reports2025
Proteomics analysis reveals FEN1 as a promising therapeutic target against small cell neuroendocrine carcinoma of the cervix.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
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Who cites it
2 citing papers in PubMed.
- Basic Clinical Bidirectional Empowerment: Synergistic Breakthrough in Molecular Mechanisms and Clinical Management of Small Cell Cervical Carcinoma.International journal of molecular sciences · 2026Review
- miR-141-5p positively regulates ACVRL1 expression to promote cervical cancer progression.Human cell · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
Small cell neuroendocrine carcinoma of the cervix (SCNECC) is a rare, aggressive cervical cancer with poor prognosis. This study explored molecular drivers of SCNECC progression and identified potential therapeutic targets. Proteomic analysis was conducted to identify differentially expressed proteins (DEPs) in SCNECC. Subsequent GO and KEGG enrichment analyses were performed to delineate key DEPs. Functional assays, including CCK-8, colony formation, cell cycle, and apoptosis assays, were conducted to assess the roles of target genes. Expression levels of target genes were validated using qRT-PCR, western blot, and immunohistochemistry (IHC). Proteomic profiling revealed 2333 DEPs in SCNECC, comprising 2168 upregulated and 165 downregulated proteins. GO and KEGG analyses revealed that the upregulated DEPs were predominantly enriched in processes occurring within the cell nucleus, such as DNA replication, reflecting heightened proliferative activity in SCNECC. IHC confirmed FEN1 overexpression. Functional assays showed that FEN1 knockdown suppressed cell viability, colony formation, and cell cycle, promoted apoptosis, and impeded tumor growth in mice. SC13, a FEN1 inhibitor, also had similar effects. Furthermore, silencing FEN1 markedly reduced PIK3CA, PCNA, and BCL-2 levels, while elevating Caspase-9 expression.
conclusionFEN1 overexpression fuels SCNECC progression via PCNA regulation, positioning FEN1 as a promising SCNECC therapeutic target.
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