Circular RNA circANKS1B acts as a sponge for miR‐152‐3p and promotes prostate cancer progression by upregulating TGF‐α expression

Background A growing number of studies indicate that circular RNAs (circRNAs) play critical roles in human diseases, and show great potential as biomarkers and therapeutic targets. This study aimed to investigate the expression and function of circANKS1B in prostate cancer (PC). Methods The expressi...

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Published in:The Prostate 2021-04, Vol.81 (5), p.271-278
Main Authors: Tao, Liang‐jun, Pan, Xin‐yuan, Wang, Jia‐wei, Zhang, Li, Tao, Ling‐song, Liang, Chao‐zhao
Format: Article
Language:English
Subjects:
Biomarkers
Cell adhesion & migration
cell invasion
Cell migration
circANKS1B
Circular RNA
miR‐152‐3p
Pheochromocytoma cells
Polymerase chain reaction
Prostate cancer
Reporter gene
Ribonucleic acid
RNA
TGF‐α
Therapeutic applications
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Summary:Background A growing number of studies indicate that circular RNAs (circRNAs) play critical roles in human diseases, and show great potential as biomarkers and therapeutic targets. This study aimed to investigate the expression and function of circANKS1B in prostate cancer (PC). Methods The expression of circANKS1B and miR‐152‐3p was analyzed by real‐time quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). Cell migration and invasion were measured using a transwell assay. The interaction between circANKS1B and miR‐152‐3p was confirmed by a dual‐luciferase reporter gene assay. Rescue experiments were conducted to determine whether circANKS1B regulated the invasion of PC cells via the circANKS1B‐miR‐152‐3p‐TGF‐α pathway. Results The expression of circANKS1B was markedly upregulated in both PC cells and tissues. Moreover, high circANKS1B expression was associated with poor prognosis in PC patients. Dual‐luciferase reporter assay indicated that circANKS1B directly bound to miR‐152‐3p. Furthermore, circANKS1B negatively regulated miR‐152‐3p expression. Knockdown of circANKS1B markedly suppressed cell migration and invasion and TGF‐α expression in PC cells, whereas the effects of circANKS1B silencing were reversed by miR‐152‐3p deficiency. In addition, the impact of miR‐152‐3p silencing on invasion of circANKS1B‐deficient PC cells was also abrogated by TGF‐α deficiency. Overall, circANKS1B acts as a sponge for miR‐152‐3p to promote PC progression by upregulating TGF‐α expression. Conclusion Our findings reveal that circANKS1B may be a potential prognostic biomarker and therapeutic target for PC.
ISSN:0270-4137
1097-0045
DOI:10.1002/pros.24102