Abstract
Prostate cancer (PCa) is one of the major men’s malignancies with high mortality worldwide. Circular RNAs (circRNAs) have been shown to serve as essential regulators in human cancers. CircRNA can exert their functions by cooperating with their host genes. In the present study, microarray analysis revealed an upregulated mRNA in PCa samples. X-linked inhibitor of apoptosis protein (XIAP), a key regulator in the progression of human cancers. Through bioinformatics analysis, we determined that XIAP is a host gene for circRNA0005276. Therefore, this study focused on the interaction between circ0005276 and XIAP as well as their functions in PCa progression. The upregulation of XIAP and circ0005276 was determined in PCa tissues and cell lines. Moreover, we confirmed the positive regulation of circ0005276 on XIAP expression. Functionally, we validated that circ0005276 and XIAP promoted cell proliferation, migration and epithelial–mesenchymal transition. Mechanistically, we verified that circ0005276 interacted with FUS binding protein (FUS) so as to activate the transcription of XIAP. Rescue assays were conducted to determine the crucial role of XIAP in circ0005276 and FUS-mediated PCa cellular processes. Collectively, our study revealed the mechanism and function of circ0005276 and its host gene XIAP in PCa progression.
Highlights
Prostate cancer (PCa), a prevalent human malignancy whose 5-year survival is merely around 29%1
Circ0005276 and X-linked inhibitor of apoptosis protein (XIAP) were upregulated in prostate cancer First of all, microarray analysis was applied to analyze the differentially expressed mRNAs in PCa tissues
XIAP was found to be a mRNA which was significantly upregulated in PCa samples
Summary
Prostate cancer (PCa), a prevalent human malignancy whose 5-year survival is merely around 29%1. The percentage of PCa in all cancer related death is about 13%2. Despite the development of comprehensive treatment, the prognosis of patients with PCa is still unfavorable due to the recurrence and metastasis[3]. As a distinct group of noncoding transcripts, circular RNAs (circRNAs), form a closed continuous loop with the. In the past 40 years, circRNAs have been identified in eukaryotic cells by electron microscopy[7,8] and were previously considered as splicing error by-products. Most circRNAs are formed by exon or intron back-splicing. This process differs from the formation of linear RNAs. Two mechanisms exist for the formation of exonic or exon–intron circRNAs: exon skipping and back-splicing[12,13].
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