PMID- 29644076
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220317
IS  - 2050-6201 (Print)
IS  - 2050-6201 (Electronic)
IS  - 2050-6201 (Linking)
VI  - 2018
IP  - 1
DP  - 2018
TI  - Lost in translation: The 3'-UTR of IGF1R as an ancient long noncoding RNA.
PG  - 82-91
LID - 10.1093/emph/eoy008 [doi]
AB  - BACKGROUND AND OBJECTIVES: The insulin-like growth factor (IGF) signaling system 
      is a major arena of intragenomic conflict over embryonic growth between imprinted 
      genes of maternal and paternal origin and the IGF type 1 receptor (IGF1R) 
      promotes proliferation of many human cancers. The 3'-untranslated region (3'-UTR) 
      of the mouse Igf1r mRNA is targeted by miR-675-3p derived from the imprinted H19 
      long noncoding RNA. We undertook a comparative sequence analysis of vertebrate 
      IGF1R 3'-UTRs to determine the evolutionary history of miR-675 target sequences 
      and to identify conserved features that are likely to be involved in 
      post-transcriptional regulation of IGF1R translation. METHODOLOGY: Sequences of 
      IGF1R 3'-UTRs were obtained from public databases and analyzed using publicly 
      available algorithms. RESULTS: A very long 3'-UTR is a conserved feature of 
      vertebrate IGF1R mRNAs. We found that some ancient microRNAs, such as let-7 and 
      mir-182, have predicted binding sites that are conserved between cartilaginous 
      fish and mammals. One very conserved region is targeted by multiple, maternally 
      expressed imprinted microRNAs that appear to have evolved more recently than the 
      targeted sequences. CONCLUSIONS AND IMPLICATIONS: The conserved structures we 
      identify in the IGF1R 3'-UTR are strong candidates for regulating cell 
      proliferation during development and carcinogenesis. These conserved structures 
      are now targeted by multiple imprinted microRNAs. These observations emphasize 
      the central importance of IGF signaling pathways in the mediation of intragenomic 
      conflicts over embryonic growth and identify possible targets for therapeutic 
      interventions in cancer.
FAU - Mainieri, Avantika
AU  - Mainieri A
AD  - Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford 
      Street, Cambridge, MA 02138, USA.
FAU - Haig, David
AU  - Haig D
AUID- ORCID: 0000-0001-7377-1605
AD  - Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford 
      Street, Cambridge, MA 02138, USA.
LA  - eng
PT  - Journal Article
DEP - 20180316
PL  - England
TA  - Evol Med Public Health
JT  - Evolution, medicine, and public health
JID - 101616698
PMC - PMC5887972
OTO - NOTNLM
OT  - H19
OT  - IGF1R
OT  - evolution
OT  - genomic imprinting
OT  - microRNA
OT  - noncoding RNA
EDAT- 2018/04/13 06:00
MHDA- 2018/04/13 06:01
PMCR- 2018/03/16
CRDT- 2018/04/13 06:00
PHST- 2017/12/10 00:00 [received]
PHST- 2018/02/21 00:00 [accepted]
PHST- 2018/04/13 06:00 [entrez]
PHST- 2018/04/13 06:00 [pubmed]
PHST- 2018/04/13 06:01 [medline]
PHST- 2018/03/16 00:00 [pmc-release]
AID - eoy008 [pii]
AID - 10.1093/emph/eoy008 [doi]
PST - epublish
SO  - Evol Med Public Health. 2018 Mar 16;2018(1):82-91. doi: 10.1093/emph/eoy008. 
      eCollection 2018.