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Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b
PURPOSE: This research concentrated on the biological effects and special mechanism of circ_0003221 in bladder cancer (BLCA). MATERIALS AND METHODS: The level quantification by reverse transcription-quantitative polymerase chain reaction was administrated for circ_0003221, microRNA-892b (miR-892b) a...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Urological Association
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9448672/ https://www.ncbi.nlm.nih.gov/pubmed/36068004 http://dx.doi.org/10.4111/icu.20220153 |
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author | Lu, Peng Jiang, Yingchun Xia, Zongyu |
author_facet | Lu, Peng Jiang, Yingchun Xia, Zongyu |
author_sort | Lu, Peng |
collection | PubMed |
description | PURPOSE: This research concentrated on the biological effects and special mechanism of circ_0003221 in bladder cancer (BLCA). MATERIALS AND METHODS: The level quantification by reverse transcription-quantitative polymerase chain reaction was administrated for circ_0003221, microRNA-892b (miR-892b) and 24-dehydrocholesterol reductase (DHCR24). The biological behaviors were assessed by EDU assay and colony formation assay for proliferation, and transwell assay for cell motility. Glycolytic metabolism was tested using the commercial kits. DHCR24 protein level and cell markers were measured through western blot. The analysis of interaction potential was conducted via dual-luciferase reporter assay and pull-down assay. Circ_0003221 was implemented via tumor xenograft assay in vivo. RESULTS: Abnormal circ_0003221 upregulation was affirmed in BLCA. BLCA cell proliferation, motility and glycolysis were impeded after circ_0003221 level was knocked down. MiR-892b was identified as a target for circ_0003221. Reduction of miR-892b relieved si-circ_0003221-induced anti-tumor response in BLCA cells. In addition, miR-892b targeted DHCR24 and circ_0003221/miR-892b could regulate the level of DHCR24. The effects of si-circ_0003221 were also counteracted by DHCR24 overexpression. CONCLUSIONS: The current evidence elucidated circ_0003221 targeted miR-892b to elevate the DHCR24 level, thus accelerating cell development and glycolytic metabolism of BLCA cells. |
format | Online Article Text |
id | pubmed-9448672 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | The Korean Urological Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-94486722022-09-13 Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b Lu, Peng Jiang, Yingchun Xia, Zongyu Investig Clin Urol Original Article PURPOSE: This research concentrated on the biological effects and special mechanism of circ_0003221 in bladder cancer (BLCA). MATERIALS AND METHODS: The level quantification by reverse transcription-quantitative polymerase chain reaction was administrated for circ_0003221, microRNA-892b (miR-892b) and 24-dehydrocholesterol reductase (DHCR24). The biological behaviors were assessed by EDU assay and colony formation assay for proliferation, and transwell assay for cell motility. Glycolytic metabolism was tested using the commercial kits. DHCR24 protein level and cell markers were measured through western blot. The analysis of interaction potential was conducted via dual-luciferase reporter assay and pull-down assay. Circ_0003221 was implemented via tumor xenograft assay in vivo. RESULTS: Abnormal circ_0003221 upregulation was affirmed in BLCA. BLCA cell proliferation, motility and glycolysis were impeded after circ_0003221 level was knocked down. MiR-892b was identified as a target for circ_0003221. Reduction of miR-892b relieved si-circ_0003221-induced anti-tumor response in BLCA cells. In addition, miR-892b targeted DHCR24 and circ_0003221/miR-892b could regulate the level of DHCR24. The effects of si-circ_0003221 were also counteracted by DHCR24 overexpression. CONCLUSIONS: The current evidence elucidated circ_0003221 targeted miR-892b to elevate the DHCR24 level, thus accelerating cell development and glycolytic metabolism of BLCA cells. The Korean Urological Association 2022-09 2022-08-23 /pmc/articles/PMC9448672/ /pubmed/36068004 http://dx.doi.org/10.4111/icu.20220153 Text en © The Korean Urological Association https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Lu, Peng Jiang, Yingchun Xia, Zongyu Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title | Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title_full | Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title_fullStr | Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title_full_unstemmed | Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title_short | Hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of DHCR24 by targeting miR-892b |
title_sort | hsa_circ_0003221 facilitates the malignant development of bladder cancer cells via resulting in the upregulation of dhcr24 by targeting mir-892b |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9448672/ https://www.ncbi.nlm.nih.gov/pubmed/36068004 http://dx.doi.org/10.4111/icu.20220153 |
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