hsa_circ0021347 as a Potential Target Regulated by B7-H3 in Modulating the Malignant Characteristics of Osteosarcoma

In our previous study, we showed that B7-H3 played crucial roles in osteosarcoma (OS) development and might serve as a negative regulator of in osteoimmunology and help tumor cells escape immune surveillance. However, little is known about B7-H3 deficiency and its corresponding circRNA alteration or...

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Bibliographic Details
Published inBioMed research international Vol. 2019; no. 2019; pp. 1 - 11
Main Authors Zhang, Long, Kang, Fu-Biao, Zhang, Guo-chuan, Wang, Ling, Zhang, Ying-ze
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 2019
Hindawi
John Wiley & Sons, Inc
Hindawi Limited
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Summary:In our previous study, we showed that B7-H3 played crucial roles in osteosarcoma (OS) development and might serve as a negative regulator of in osteoimmunology and help tumor cells escape immune surveillance. However, little is known about B7-H3 deficiency and its corresponding circRNA alteration or their relationship with osteosarcoma progression. Therefore, we established stable silencing of B7-H3 in OS cells and validated our results with western blotting and real-time PCR detection. Then, we performed a circRNA array to analyze the differential expression of circRNAs between the control and B7-H3 knockdown cells. The association between target circRNA expression and the clinicopathological features of patients with OS was further analyzed. As a result, hsa_circ0021347 was selected and validated to be significantly downregulated in OS tissues and cell lines and showed a strong negative relationship with B7-H3 expression in OS. In addition, clinicopathological features showed that hsa_circ0021347 in OS tissues was negatively associated with Enneking stage and positively associated with patients’ survival. Finally, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and PANTHER pathway analyses were performed to predict a network of hsa_circ0021347/miRNAs interactions to help us develop potential biomarkers for clinical diagnosis and design therapeutic strategies for OS.
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Academic Editor: Susan A. Rotenberg
ISSN:2314-6133
2314-6141
DOI:10.1155/2019/9301989