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. 2021 Jul 22;12(8):726. doi: 10.1038/s41419-021-04015-w

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© The Author(s) 2021, corrected publication 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A Sanger sequencing identified the back-splicing site of hsa_circ_0001747. B Basal expression level of hsa_circ_0001747 in PCa cell lines. C Hsa_circ_0001747 was resistant to RNase R digestion. D Electrophoresis confirmed hsa_circ_0001747 was amplified in cDNA instead of gDNA samples. E Hsa_circ_0001747 was mainly distributed in the cytoplasm in PCa cells. F RT-qPCR verified the transfection efficiency of siRNAs targeting to hsa_circ_0001747 in DU145 and 22Rv1. G CCK-8 assay verified knockdown of hsa_circ_0001747 promoted PCa cells viability. H Knockdown of hsa_circ_0001747 facilitated colony formation in PCa cells. I Knockdown of hsa_circ_0001747 promoted the subcutaneous tumor growth in nude mice. Error bar indicates mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.