Abstract
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.
Key Indexing Terms
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Article info
Publication history
Published online: August 21, 2022
Accepted:
August 15,
2022
Received:
August 13,
2021
Identification
Copyright
© 2022 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.
