PMID- 34298972
OWN - NLM
STAT- MEDLINE
DCOM- 20210817
LR  - 20210817
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 22
IP  - 14
DP  - 2021 Jul 8
TI  - Role of miR-24 in Multiple Endocrine Neoplasia Type 1: A Potential Target for 
      Molecular Therapy.
LID - 10.3390/ijms22147352 [doi]
LID - 7352
AB  - 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.
FAU - Marini, Francesca
AU  - Marini F
AD  - Department of Experimental and Clinical Biomedical Sciences, University of 
      Florence, Viale Pieraccini 6, 50139 Florence, Italy.
AD  - F.I.R.M.O., Italian Foundation for the Research on Bone Diseases, Via Reginaldo 
      Giuliani 195/A, 50141 Florence, Italy.
FAU - Brandi, Maria Luisa
AU  - Brandi ML
AUID- ORCID: 0000-0002-8741-0592
AD  - F.I.R.M.O., Italian Foundation for the Research on Bone Diseases, Via Reginaldo 
      Giuliani 195/A, 50141 Florence, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210708
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Antagomirs)
RN  - 0 (MEN1 protein, human)
RN  - 0 (MIRN24 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Animals
MH  - Antagomirs/pharmacology/therapeutic use
MH  - Chromosomes, Human, Pair 19/genetics
MH  - Chromosomes, Human, Pair 9/genetics
MH  - DNA Damage
MH  - Feedback, Physiological
MH  - Forecasting
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Regulatory Networks
MH  - *Genetic Therapy
MH  - Humans
MH  - MicroRNAs/*genetics
MH  - *Molecular Targeted Therapy
MH  - Multiple Endocrine Neoplasia Type 1/*genetics/metabolism/therapy
MH  - Neoplasm Proteins/antagonists & inhibitors/genetics/metabolism
MH  - Neoplasms/genetics/metabolism/pathology
MH  - Protein Isoforms/genetics
MH  - Proto-Oncogene Proteins/antagonists & inhibitors/genetics/metabolism
MH  - RNA, Messenger/antagonists & inhibitors/genetics
MH  - RNA, Neoplasm/antagonists & inhibitors/genetics
MH  - Rats
PMC - PMC8306915
OTO - NOTNLM
OT  - MEN1 gene
OT  - loss of heterozygosity (LOH)
OT  - miR-24
OT  - microRNA (miRNAs)
OT  - multiple endocrine neoplasia type 1 (MEN1)
COIS- The authors declare no conflict of interest.
EDAT- 2021/07/25 06:00
MHDA- 2021/08/18 06:00
PMCR- 2021/07/08
CRDT- 2021/07/24 01:01
PHST- 2021/06/16 00:00 [received]
PHST- 2021/07/07 00:00 [revised]
PHST- 2021/07/07 00:00 [accepted]
PHST- 2021/07/24 01:01 [entrez]
PHST- 2021/07/25 06:00 [pubmed]
PHST- 2021/08/18 06:00 [medline]
PHST- 2021/07/08 00:00 [pmc-release]
AID - ijms22147352 [pii]
AID - ijms-22-07352 [pii]
AID - 10.3390/ijms22147352 [doi]
PST - epublish
SO  - Int J Mol Sci. 2021 Jul 8;22(14):7352. doi: 10.3390/ijms22147352.