Implication of TrkC-miR2 in neurotrophin signalling pathway regulation through NGFR transcript targeting.
NGFR
TrkC-miR2
neurotrophin signalling pathway
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
revised:
29
01
2021
received:
15
10
2020
accepted:
15
02
2021
pubmed:
7
3
2021
medline:
18
9
2021
entrez:
6
3
2021
Statut:
ppublish
Résumé
TrkC and NGFR neurotrophin receptors are associated with cell death, cancer and differentiation. TrkC-miR2, which is located in TrkC gene, is known to regulate Wnt signalling pathway, and its influence on other signalling pathways is under investigation. Here, through RT-qPCR, dual-luciferase assay and Western blotting we reveal that TrkC-miR2 targets NGFR. Overexpression of TrkC-miR2 also affected TrkA, TrkC, NFKB, BCL2 and Akt2 expressions involved in neurotrophin signalling pathway, and elevated survival rate of HEK293t and U87 cells was distinguished by flow cytometry and MTT assay. Consistently, an opposite expression correlation was obtained between TrkC-miR2 and NGFR or TrkC for the duration of NT2 differentiation. Meanwhile, TrkC-miR2 down-regulation attenuated NT2 differentiation into neural-like cells. Overall, here we present in silico and experimental evidence showing TrkC-miR2 as a new controller in regulation of neurotrophin signalling pathway.
Identifiants
pubmed: 33675128
doi: 10.1111/jcmm.16415
pmc: PMC8034437
doi:
Substances chimiques
MicroRNAs
0
NGFR protein, human
0
NTRK3 protein, human
0
Nerve Growth Factors
0
Nerve Tissue Proteins
0
Receptors, Nerve Growth Factor
0
Receptor, trkC
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3381-3390Subventions
Organisme : INSF (grant NO. 96012144) and Tarbiat Modares University
Informations de copyright
© 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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