CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13

Abstract Background Prostate cancer (PCa) belongs to an epithelial malignancy that occurs in the prostate gland and is the most common malignancy of the male genitourinary system. Referring to related literature, circSERPINA3 has been reported to be up-regulated in PCa. However, its biological funct...

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Autores principales:	Zengshu Xing, Sailian Li, Zhenxiang Liu, Chong Zhang, Zhiming Bai
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	circSERPINA3 SERPINA3 miR-653-5p BUD13 Prostate cancer Medicine R
Acceso en línea:	https://doaj.org/article/87d008945f604d588c0d9bff66ce9fd1
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spelling	oai:doaj.org-article:87d008945f604d588c0d9bff66ce9fd12021-12-05T12:05:57ZCircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD1310.1186/s12967-021-03063-21479-5876https://doaj.org/article/87d008945f604d588c0d9bff66ce9fd12021-12-01T00:00:00Zhttps://doi.org/10.1186/s12967-021-03063-2https://doaj.org/toc/1479-5876Abstract Background Prostate cancer (PCa) belongs to an epithelial malignancy that occurs in the prostate gland and is the most common malignancy of the male genitourinary system. Referring to related literature, circSERPINA3 has been reported to be up-regulated in PCa. However, its biological function remains unclear. Purpose This study aimed to reveal the specific role and relevant molecular mechanism of circSERPINA3 in PCa. Methods RT-qPCR was used to examine gene expression and functional analyses were conducted to verify the effect of circSERPINA3 on cell apoptosis, autophagy and aerobic glycolysis in PCa cells. Mechanism assays were applied to evaluate the relationship among circSERPINA3/miR-653-5p/SERPINA3/BUD13. Results CircSERPINA3 was verified to be up-regulated in PCa cells and to inhibit cell apoptosis while promoting aerobic glycolysis and autophagy in PCa cells. CircSERPINA3 and SERPINA3 were also testified to bind to miR-653-5p through a line of mechanism experiments. Moreover, it was discovered that circSERPINA3 could stabilize SERPINA3 mRNA via recruiting BUD13. Additionally, SERPINA3 was verified to inhibit cell apoptosis, while promoting aerobic glycolysis and autophagy in PCa cells. Conclusions Our study suggested that circSERPINA3 regulated apoptosis, autophagy and aerobic glycolysis of PCa cells by competitively binding to miR-653-5p and recruiting BUD13. Graphic abstractZengshu XingSailian LiZhenxiang LiuChong ZhangZhiming BaiBMCarticlecircSERPINA3SERPINA3miR-653-5pBUD13Prostate cancerMedicineRENJournal of Translational Medicine, Vol 19, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	circSERPINA3 SERPINA3 miR-653-5p BUD13 Prostate cancer Medicine R
spellingShingle	circSERPINA3 SERPINA3 miR-653-5p BUD13 Prostate cancer Medicine R Zengshu Xing Sailian Li Zhenxiang Liu Chong Zhang Zhiming Bai CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
description	Abstract Background Prostate cancer (PCa) belongs to an epithelial malignancy that occurs in the prostate gland and is the most common malignancy of the male genitourinary system. Referring to related literature, circSERPINA3 has been reported to be up-regulated in PCa. However, its biological function remains unclear. Purpose This study aimed to reveal the specific role and relevant molecular mechanism of circSERPINA3 in PCa. Methods RT-qPCR was used to examine gene expression and functional analyses were conducted to verify the effect of circSERPINA3 on cell apoptosis, autophagy and aerobic glycolysis in PCa cells. Mechanism assays were applied to evaluate the relationship among circSERPINA3/miR-653-5p/SERPINA3/BUD13. Results CircSERPINA3 was verified to be up-regulated in PCa cells and to inhibit cell apoptosis while promoting aerobic glycolysis and autophagy in PCa cells. CircSERPINA3 and SERPINA3 were also testified to bind to miR-653-5p through a line of mechanism experiments. Moreover, it was discovered that circSERPINA3 could stabilize SERPINA3 mRNA via recruiting BUD13. Additionally, SERPINA3 was verified to inhibit cell apoptosis, while promoting aerobic glycolysis and autophagy in PCa cells. Conclusions Our study suggested that circSERPINA3 regulated apoptosis, autophagy and aerobic glycolysis of PCa cells by competitively binding to miR-653-5p and recruiting BUD13. Graphic abstract
format	article
author	Zengshu Xing Sailian Li Zhenxiang Liu Chong Zhang Zhiming Bai
author_facet	Zengshu Xing Sailian Li Zhenxiang Liu Chong Zhang Zhiming Bai
author_sort	Zengshu Xing
title	CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
title_short	CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
title_full	CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
title_fullStr	CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
title_full_unstemmed	CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13
title_sort	circserpina3 regulates serpina3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to mir-653-5p and recruiting bud13
publisher	BMC
publishDate	2021
url	https://doaj.org/article/87d008945f604d588c0d9bff66ce9fd1
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CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13

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