ArticlePloS one2012
The negative feedback-loop between the oncomir Mir-24-1 and menin modulates the Men1 tumorigenesis by mimicking the "Knudson's second hit".
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review.Mutation research. Reviews in mutation researchPooled it
- [A combination of endogenous hypercortisolism and primary hyperparathyroidism: clinical and genetic characteristics].Problemy endokrinologii · 2026Observational
- Two novel multiple endocrine neoplasia type 1 variants caused thymic neuroendocrine tumor: a case report.Hereditary cancer in clinical practice · 2026Article
- Familial MEN1 Syndrome with Atypical Renal Features and a Coexisting CLDN16 Variant: A Case Series.Journal of clinical medicine · 2025Article
- Serums miR-24-3p and miR-1301-3p as Potential Biomarkers in MEN1 Syndrome.International journal of molecular sciences · 2025Article
- [The role of immunosurveillance and immunoediting in hereditary cancer predisposition syndromes].Magyar onkologia · 2025Review
- Molecular Pathophysiology of Parathyroid Tumorigenesis-The Lesson from a Rare Disease: The "MEN1 Model".International journal of molecular sciences · 2024Review
- Menin in Cancer.Genes · 2024Review
- Childhood Multiple Endocrine Neoplasia (MEN) Syndromes: Genetics, Clinical Heterogeneity and Modifying Genes.Journal of clinical medicine · 2024Review
- [Plasma miRNA expression in patients with genetically confirmed multiple endocrine neoplasia type 1 syndrome and its phenocopies].Problemy endokrinologii · 2024Article
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Loss of tumor suppressor menin expression in high grade cholangiocarcinomas.BMC research notes · 2023Article
- miR-3156-5p is downregulated in serum of MEN1 patients and regulates expression of MORF4L2.Endocrine-related cancer · 2022Article
- MicroRNA Profile Alterations in Parathyroid Carcinoma: Latest Updates and Perspectives.Cancers · 2022Review
- Epigenetic Regulation in Gastroenteropancreatic Neuroendocrine Tumors.Frontiers in oncology · 2022Review
- [Morphological characteristics of pituitary adenomas in the phenocopy of multiple endocrine neoplasia type 1].Problemy endokrinologii · 2021Article
- Parathyroid Tumors: Molecular Signatures.International journal of molecular sciences · 2021Review
- Are Non-Coding RNAs Useful Biomarkers in Parathyroid Tumorigenesis?International journal of molecular sciences · 2021Review
- Role of miR-24 in Multiple Endocrine Neoplasia Type 1: A Potential Target for Molecular Therapy.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple endocrine neoplasia type 1 (MEN1) syndrome is a rare hereditary cancer disorder characterized by tumors of the parathyroids, of the neuroendocrine cells, of the gastro-entero-pancreatic tract, of the anterior pituitary, and by non-endocrine neoplasms and lesions. MEN1 gene, a tumor suppressor gene, encodes menin protein. Loss of heterozygosity at 11q13 is typical of MEN1 tumors, in agreement with the Knudson's two-hit hypothesis. In silico analysis with Target Scan, Miranda and Pictar-Vert softwares for the prediction of miRNA targets indicated miR-24-1 as capable to bind to the 3'UTR of MEN1 mRNA. We investigated this possibility by analysis of miR-24-1 expression profiles in parathyroid adenomatous tissues from MEN1 gene mutation carriers, in their sporadic non-MEN1 counterparts, and in normal parathyroid tissue. Interestingly, the MEN1 tumorigenesis seems to be under the control of a "negative feedback loop" between miR-24-1 and menin protein, that mimics the second hit of Knudson's hypothesis and that could buffer the effect of the stochastic factors that contribute to the onset and progression of this disease. Our data show an alternative way to MEN1 tumorigenesis and, probably, to the "two-hit dogma". The functional significance of this regulatory mechanism in MEN1 tumorigenesis is also the basis for opening future developments of RNA antagomir(s)-based strategies in the in vivo control of tumorigenesis in MEN1 carriers.
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