PMID- 29615472
OWN - NLM
STAT- MEDLINE
DCOM- 20191028
LR  - 20191028
IS  - 1479-6813 (Electronic)
IS  - 0952-5041 (Print)
IS  - 0952-5041 (Linking)
VI  - 61
IP  - 1
DP  - 2018 Jul
TI  - Epigenetic regulation in the tumorigenesis of MEN1-associated endocrine cell 
      types.
PG  - R13-R24
LID - JME-18-0050 [pii]
LID - 10.1530/JME-18-0050 [doi]
AB  - Epigenetic regulation is emerging as a key feature in the molecular 
      characteristics of various human diseases. Epigenetic aberrations can occur from 
      mutations in genes associated with epigenetic regulation, improper deposition, 
      removal or reading of histone modifications, DNA methylation/demethylation and 
      impaired non-coding RNA interactions in chromatin. Menin, the protein product of 
      the gene causative for the multiple endocrine neoplasia type 1 (MEN1) syndrome, 
      interacts with chromatin-associated protein complexes and also regulates some 
      non-coding RNAs, thus participating in epigenetic control mechanisms. Germline 
      inactivating mutations in the MEN1 gene that encodes menin predispose patients to 
      develop endocrine tumors of the parathyroids, anterior pituitary and the 
      duodenopancreatic neuroendocrine tissues. Therefore, functional loss of menin in 
      the various MEN1-associated endocrine cell types can result in epigenetic changes 
      that promote tumorigenesis. Because epigenetic changes are reversible, they can 
      be targeted to develop therapeutics for restoring the tumor epigenome to the 
      normal state. Irrespective of whether epigenetic alterations are the cause or 
      consequence of the tumorigenesis process, targeting the endocrine 
      tumor-associated epigenome offers opportunities for exploring therapeutic 
      options. This review presents epigenetic control mechanisms relevant to the 
      interactions and targets of menin, and the contribution of epigenetics in the 
      tumorigenesis of endocrine cell types from menin loss.
CI  - (c) 2018 Society for Endocrinology.
FAU - Iyer, Sucharitha
AU  - Iyer S
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, NIH, Bethesda, Maryland, USA.
FAU - Agarwal, Sunita K
AU  - Agarwal SK
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, NIH, Bethesda, Maryland, USA.
LA  - eng
GR  - Z99 DK999999/Intramural NIH HHS/United States
GR  - ZIA DK075035-01/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PT  - Review
DEP - 20180403
PL  - England
TA  - J Mol Endocrinol
JT  - Journal of molecular endocrinology
JID - 8902617
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Cell Transformation, Neoplastic/genetics/metabolism
MH  - Epigenesis, Genetic/*genetics
MH  - Humans
MH  - Multiple Endocrine Neoplasia Type 1/genetics/*metabolism
MH  - Neuroendocrine Tumors/genetics/metabolism
MH  - Transcription Factors/genetics/metabolism
PMC - PMC5966343
MID - NIHMS958260
OTO - NOTNLM
OT  - neuroendocrine
OT  - pancreas
OT  - parathyroid
OT  - pituitary
COIS- Declaration of interest: The authors declare that there is no conflict of 
      interest that could be perceived as prejudicing the impartiality of this review.
EDAT- 2018/04/05 06:00
MHDA- 2019/10/29 06:00
PMCR- 2019/07/01
CRDT- 2018/04/05 06:00
PHST- 2018/02/18 00:00 [received]
PHST- 2018/04/03 00:00 [accepted]
PHST- 2018/04/05 06:00 [pubmed]
PHST- 2019/10/29 06:00 [medline]
PHST- 2018/04/05 06:00 [entrez]
PHST- 2019/07/01 00:00 [pmc-release]
AID - JME-18-0050 [pii]
AID - 10.1530/JME-18-0050 [doi]
PST - ppublish
SO  - J Mol Endocrinol. 2018 Jul;61(1):R13-R24. doi: 10.1530/JME-18-0050. Epub 2018 Apr 
      3.