CircDHDDS/miR-361-3p/WNT3A Axis Promotes the Development of Retinoblastoma by Regulating Proliferation, Cell Cycle, Migration, and Invasion of Retinoblastoma Cells.
Adolescent
Cell Cycle
/ physiology
Cell Line, Tumor
Cell Movement
/ physiology
Cell Proliferation
/ physiology
Child
Female
Gene Expression Regulation, Neoplastic
/ physiology
Humans
Male
MicroRNAs
/ metabolism
RNA, Circular
/ metabolism
Retinoblastoma
/ metabolism
Wnt3A Protein
/ metabolism
Young Adult
Circular RNA
RB
WNT3A
circDHDDS
miR-361-3p
Journal
Neurochemical research
ISSN: 1573-6903
Titre abrégé: Neurochem Res
Pays: United States
ID NLM: 7613461
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
03
01
2020
accepted:
13
08
2020
revised:
09
08
2020
pubmed:
1
9
2020
medline:
3
6
2021
entrez:
1
9
2020
Statut:
ppublish
Résumé
Retinoblastoma (RB) is a common intraocular malignant tumor. The growing evidence has reported that circular RNAs (circRNAs) play critical roles in RB development. Therefore, the purpose of the study is to investigate the regulatory mechanism of circDHDDS in RB. The real-time quantitative polymerase chain reaction (RT-qPCR) assay was used to quantify the expression levels of circDHDDS, miR-361-3p, and WNT3A in RB tissues and cells (RPCs, Y-79, and WERI-Rb-1). The proliferation and cell cycle of RB cells were assessed by colony formation assay and flow cytometry assays, respectively. The migration and invasion of RB cells were measured by transwell assay. The protein expression levels of Nectin-3 (CD113), SOX2, Nanog, and WNT3A were measured by Western blot assay. The functional targets of circDHDDS and miR-361-3p were predicted by bioinformatics databases, and the dual-luciferase reporter assay was used to confirm the interaction relationship between miR-361-3p and circDHDDS or WNT3A. The functional role of circDHDDS silencing in vivo was evaluated by xenograft experiment. We found that circDHDDS was overexpressed in RB tissues and cells compared with normal retinas tissues and retinal pigment epithelial cells, correspondingly. Furthermore, silencing of circDHDDS impeded proliferation, migration, invasion, and induced cell cycle arrest in vitro, which were abolished by knockdown of miR-361-3p. The in vivo experiments also suggested that tumor growth was inhibited by knockdown of circDHDDS. Moreover, we also found that miR-361-3p specifically bound to WNT3A, and overexpression of miR-361-3p suppressed RB development by decreasing WNT3A expression. Summarily, circDHDDS, a molecule sponge of miR-361-3p, regulated the expression of WNT3A. Therefore, circDHDDS/miR-361-3p/WNT3A axis stimulated the development of RB by regulation of proliferation, cell cycle program, migration, and invasion of RB cells.
Identifiants
pubmed: 32865704
doi: 10.1007/s11064-020-03112-0
pii: 10.1007/s11064-020-03112-0
doi:
Substances chimiques
MIRN361 microRNA, human
0
MicroRNAs
0
RNA, Circular
0
WNT3A protein, human
0
Wnt3A Protein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2691-2702Références
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