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Published on: August 23, 2019
Role of miR-24 in Multiple Endocrine Neoplasia Type 1: A Potential Target for Molecular Therapy
Francesca Marini1,2, Maria Luisa Brandi2
1Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy.
Abstract:
Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant inherited multiple cancer syndrome of neuroendocrine tissues. Tumors are caused by an inherited germinal heterozygote inactivating mutation of the MEN1 tumor suppressor gene, followed by a somatic loss of heterozygosity (LOH) of the MEN1 gene in target neuroendocrine cells, mainly at parathyroids, pancreas islets, and anterior pituitary. Over 1500 different germline and somatic mutations of the MEN1 gene have been identified, but the syndrome is completely missing a direct genotype-phenotype correlation, thus supporting the hypothesis that exogenous and endogenous factors, other than MEN1 specific mutation, are involved in MEN1 tumorigenesis and definition of individual clinical phenotype. Epigenetic factors, such as microRNAs (miRNAs), are strongly suspected to have a role in MEN1 tumor initiation and development. Recently, a direct autoregulatory network between miR-24, MEN1 mRNA, and menin was demonstrated in parathyroids and endocrine pancreas, showing a miR-24-induced silencing of menin expression that could have a key role in initiation of tumors in MEN1-target neuroendocrine cells. Here, we review the current knowledge on the post-transcriptional regulation of MEN1 and menin expression by miR-24, and its possible direct role in MEN1 syndrome, describing the possibility and the potential approaches to target and silence this miRNA, to permit the correct expression of the wild type menin, and thereby prevent the development of cancers in the target tissues.
Insights
Multiple endocrine neoplasia type 1 (MEN1) is a rare cancer syndrome. MiR-24 may drive MEN1 tumor development by silencing menin expression, suggesting therapeutic targeting of this miRNA.
Area of Science:
- Endocrinology
- Oncology
- Genetics
Background:
- Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant inherited cancer syndrome affecting neuroendocrine tissues.
- Tumors arise from inactivating mutations in the MEN1 tumor suppressor gene, but genotype-phenotype correlations are lacking, suggesting other factors influence tumorigenesis.
- Epigenetic factors, like microRNAs (miRNAs), are implicated in MEN1 tumor initiation and progression.
Purpose of the Study:
- To review the role of post-transcriptional regulation by miR-24 in MEN1 syndrome.
- To explore the autoregulatory network between miR-24, MEN1 mRNA, and menin.
- To discuss potential therapeutic strategies targeting miR-24 to prevent MEN1-associated cancers.
Main Methods:
- Literature review of current knowledge on miR-24 and MEN1.
- Analysis of the autoregulatory network involving miR-24, MEN1 mRNA, and menin.
- Discussion of potential therapeutic approaches targeting miR-24.
Main Results:
- A direct autoregulatory network between miR-24, MEN1 mRNA, and menin has been identified in parathyroids and endocrine pancreas.
- miR-24 induces silencing of menin expression, potentially playing a key role in initiating tumors in MEN1-target neuroendocrine cells.
- Over 1500 MEN1 gene mutations are known, yet a direct genotype-phenotype correlation is absent.
Conclusions:
- miR-24-mediated silencing of menin is a potential key factor in MEN1 tumorigenesis.
- Targeting and silencing miR-24 could restore wild-type menin expression and prevent cancer development in MEN1 patients.
- Further research into miR-24's role may lead to novel therapeutic strategies for MEN1 syndrome.
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