ArticleJournal of experimental & clinical cancer research : CR2017
Musashi-2, a novel oncoprotein promoting cervical cancer cell growth and invasion, is negatively regulated by p53-induced miR-143 and miR-107 activation.
Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Pooled it
- Review
- Differentially Expressed Genes Associated with the Development of Cervical Cancer.International journal of molecular sciences · 2025Article
- miR-107 repressesMolecular therapy. Nucleic acids · 2025Article
- A Critical Review on microRNAs as Prognostic Biomarkers in Laryngeal Carcinoma.International journal of molecular sciences · 2024Review
- Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2.Oncology reports · 2024Article
- Jolkinolide B inhibits the progression of hepatocellular carcinoma by regulating Musashi-2 protein.PloS one · 2024Article
- MicroRNA-Mediated Regulation of Histone-Modifying Enzymes in Cancer: Mechanisms and Therapeutic Implications.Biomolecules · 2023Review
- The Musashi RNA-binding proteins in female cancers: insights on molecular mechanisms and therapeutic relevance.Biomarker research · 2023Review
- MicroRNA-143 acts as a tumor suppressor through Musashi-2/DLL1/Notch1 and Musashi-2/Snail1/MMPs axes in acute myeloid leukemia.Journal of translational medicine · 2023Article
- First insight into extracellular vesicle-miRNA characterization in a sheepFrontiers in veterinary science · 2023Article
- Role of the RNA-binding protein family in gynecologic cancers.American journal of cancer research · 2023Review
- Review
- [Advances in research of Musashi2 in solid tumors].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Review
- Infection by High-Risk Human Papillomaviruses, Epithelial-to-Mesenchymal Transition and Squamous Pre-Malignant or Malignant Lesions of the Uterine Cervix: A Series of Chained Events?International journal of molecular sciences · 2021Review
- Article
- Mithramycin delivery systems to develop effective therapies in sarcomas.Journal of nanobiotechnology · 2021Article
- The role of HPV-induced epigenetic changes in cervical carcinogenesis (Review).Biomedical reports · 2021Review
- LncRNA CARMN overexpression promotes prognosis and chemosensitivity of triple negative breast cancer via acting as miR143-3p host gene and inhibiting DNA replication.Journal of experimental & clinical cancer research : CR · 2021Article
- Musashi 2 influences chronic lymphocytic leukemia cell survival and growth making it a potential therapeutic target.Leukemia · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough previous studies have shown promise for targeting Musashi RNA-binding protein 2 (MSI-2) in diverse tumors, the role and mechanism of MSI-2 for cervical cancer (CC) progression and the regulation of MSI-2 expression remains unclear.
methodsUsing gene expression and bioinformatic analysis, together with gain- and loss-of-function assays, we identified MSI-2 as a novel oncogenic driver and a poor prognostic marker in CC. We explored the regulation of c-FOS by MSI-2 via RNA-immunoprecipitation and luciferase assay, and confirmed a direct inhibition of MSI-2 by miR-143/miR-107 using luciferase assay. We assessed the effect of a natural antibiotic Mithramycin A on p53, miR-143/miR-107 and MSI-2 expression in CC cells.
resultsMSI-2 mRNA is highly expressed in CC tissues and its overexpression correlates with lower overall survival. MSI-2 promotes CC cell growth, invasiveness and sphere formation through directly binding to c-FOS mRNA and by increasing c-FOS protein expression. Furthermore, miR-143/miR-107 are two tumor suppressor miRNAs that directly bind and inhibit MSI-2 expression in CC cells, and downregulation of miR-143/miR-107 associates with poor patient prognosis. Importantly, we found that p53 decreases the expression of MSI-2 through elevating miR-143/miR-107 levels, and treatment with a natural antibiotic Mithramycin A increased p53 and miR-143/miR-107 expression and reduced MSI-2 expression, resulting in the inhibition of CC cell proliferation, invasion and sphere formation.
conclusionsThese results suggest that MSI-2 plays a crucial role in promoting the aggressive phenotypes of CC cells, and restoration of miR-143/miR-107 by Mithramycin A via activation of p53 may represent a novel therapeutic approach for CC.
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