ArticleJournal of ovarian research2022
miR-4324 inhibits ovarian cancer progression by targeting FEN1.
Article in Journal of ovarian research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- HAUS1-mediated activation of CDK4 transcription enhances proliferation, invasion and migration in hepatocellular carcinoma.Cancer gene therapy · 2026Article
- Review
- LINC01002 functions as a ceRNA to regulate FRMD8 by sponging miR-4324 for the development of COVID-19.Virology journal · 2024Article
- The endonuclease FEN1 mediates activation of STAT3 and facilitates proliferation and metastasis in breast cancer.Molecular biology reports · 2024Article
- The significance of HAUS1 and its relationship with immune microenvironment in hepatocellular carcinoma.Journal of Cancer · 2024Article
- CircUBE2D2 regulates HMGB1 through miR-885-5p to promote ovarian cancer malignancy.Clinics (Sao Paulo, Brazil) · 2024Article
- Whole transcriptome analysis revealed the regulatory network and related pathways of non-coding RNA regulating ovarian atrophy in broody hens.Frontiers in veterinary science · 2024Article
- A mitochondria-related genes associated neuroblastoma signature - based on bulk and single-cell transcriptome sequencing data analysis, and experimental validation.Frontiers in immunology · 2024Article
- [Expression of miR-4324 and its targeted gene Talin2 in breast cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian cancer is one of the most lethal malignancies, with a 1.9% mortality rate worldwide. The dysregulation of the FEN1 gene and miR-4324 has been associated with cancer progression. However, the relationship between miR-4324 and-FEN1 requires further investigation.
methodsmiR-4324 and FEN1 expressions in ovarian cancer tissues and cell lines were measured via RT-qPCR. The interaction between miR-4324 and FEN1 was assessed using luciferase and RNA pull-down assays. The effects of miR-4324 and FEN1 on cell proliferation, adhesion and apoptosis were determined by CCK-8, BrdU, colony formation, cell adhesion, Caspase-3 and western blot assays in ovarian cancer cell lines CaOV3 and OVCAR3, respectively.
resultsThe results showed that miR-4324 expression was significantly decreased and FEN1 expression was enhanced in ovarian cancer tissues and cell lines. miR-4324 inhibitor promoted cell proliferation, adhesion and migration, and prevented apoptosis. Furthermore, the downregulation of FEN1 inhibited ovarian cancer cell growth and increased apoptosis. miR-4324 inhibited FEN1 expression and repressed ovarian cancer progression.
conclusionOur study found that miR-4324 inhibited FEN1 expression, suppressed cell growth, and increased apoptosis in ovarian cancer cells. Therefore, we identified miR-4324 and FEN1 as potential therapeutic targets for ovarian cancer treatment.
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