LncRNA ATP1A1-AS1 inhibits cell proliferation and promotes cell apoptosis in thyroid carcinoma by regulating the miR-620/IRF2BP2 axis.
Humans
RNA, Long Noncoding
/ genetics
Cell Line, Tumor
MicroRNAs
/ genetics
Thyroid Neoplasms
/ genetics
Cell Proliferation
/ genetics
Apoptosis
/ genetics
Gene Expression Regulation, Neoplastic
DNA-Binding Proteins
/ genetics
Transcription Factors
/ genetics
Sodium-Potassium-Exchanging ATPase
/ genetics
ATP1A1-AS1
IRF2BP2
Thyroid carcinoma
miR-620
Journal
The American journal of the medical sciences
ISSN: 1538-2990
Titre abrégé: Am J Med Sci
Pays: United States
ID NLM: 0370506
Informations de publication
Date de publication:
01 2023
01 2023
Historique:
received:
13
08
2021
revised:
28
02
2022
accepted:
15
08
2022
pubmed:
25
8
2022
medline:
4
1
2023
entrez:
24
8
2022
Statut:
ppublish
Résumé
Thyroid carcinoma (THCA) is a common malignancy of the endocrine system. Further understanding of the molecular mechanism underlying THCA is crucial to develop effective diagnostic therapy and improve its treatments. In this study, we intended to provide novel direction for THCA targeted therapy from the aspect of lncRNA-miRNA-mRNA interaction. We aimed to investigate the function and molecular mechanism of lncRNA ATP1A1-AS1 in THCA. Gene expression was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell growth was detected by CCK-8 and EdU assays. Flow cytometry was applied for analyzing cell apoptosis. The binding of ATP1A1-AS1 or IRF2BP2 to miR-620 was validated by RNA pulldown and luciferase reporter assays. The protein levels were examined by western blotting. ATP1A1-AS1 was decreased in THCA cells and tissues. ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis. LncRNA ATP1A1-AS1 inhibited cell growth and promotes apoptosis in THCA via the miR-620/IRF2BP2 axis.
Sections du résumé
BACKGROUND
Thyroid carcinoma (THCA) is a common malignancy of the endocrine system. Further understanding of the molecular mechanism underlying THCA is crucial to develop effective diagnostic therapy and improve its treatments. In this study, we intended to provide novel direction for THCA targeted therapy from the aspect of lncRNA-miRNA-mRNA interaction. We aimed to investigate the function and molecular mechanism of lncRNA ATP1A1-AS1 in THCA.
METHODS
Gene expression was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell growth was detected by CCK-8 and EdU assays. Flow cytometry was applied for analyzing cell apoptosis. The binding of ATP1A1-AS1 or IRF2BP2 to miR-620 was validated by RNA pulldown and luciferase reporter assays. The protein levels were examined by western blotting.
RESULTS
ATP1A1-AS1 was decreased in THCA cells and tissues. ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis.
CONCLUSIONS
LncRNA ATP1A1-AS1 inhibited cell growth and promotes apoptosis in THCA via the miR-620/IRF2BP2 axis.
Identifiants
pubmed: 36002076
pii: S0002-9629(22)00346-9
doi: 10.1016/j.amjms.2022.08.005
pii:
doi:
Substances chimiques
RNA, Long Noncoding
0
MicroRNAs
0
IRF2BP2 protein, human
0
DNA-Binding Proteins
0
Transcription Factors
0
ATP1A1 protein, human
EC 3.6.1.-
Sodium-Potassium-Exchanging ATPase
EC 7.2.2.13
MIRN620 microRNA, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
73-83Informations de copyright
Copyright © 2022 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interests The authors declare that there are no competing interests in this study.