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Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression
BACKGROUND: Circular RNAs (circRNAs) take part in colorectal cancer malignancies. CircRNA dedicator of cytokinesis 1 (circ_DOCK1) is involved in colorectal cancer progression, but the mechanism underlying this circRNA that takes part in colorectal cancer development remains largely undetermined. MET...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941900/ https://www.ncbi.nlm.nih.gov/pubmed/33685455 http://dx.doi.org/10.1186/s12957-021-02173-x |
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author | Zhang, Weitong Wang, Zhenfen Cai, Guohao Huang, Ping |
author_facet | Zhang, Weitong Wang, Zhenfen Cai, Guohao Huang, Ping |
author_sort | Zhang, Weitong |
collection | PubMed |
description | BACKGROUND: Circular RNAs (circRNAs) take part in colorectal cancer malignancies. CircRNA dedicator of cytokinesis 1 (circ_DOCK1) is involved in colorectal cancer progression, but the mechanism underlying this circRNA that takes part in colorectal cancer development remains largely undetermined. METHODS: Tumor and normal para-cancerous tissues were collected from 42 colorectal cancer patients. Human colorectal cancer cell lines (HCT116 and SW480) were used for the experiments in vitro. Circ_DOCK1, microRNA (miR)-132-3p, and ubiquitin-specific protease 11 (USP11) levels were measured through quantitative real-time polymerase chain reaction and Western blotting. Cell growth, metastasis, and apoptosis were investigated via colony formation, 5-ethynyl-2′-deoxyuridine (EdU) staining, MTT, flow cytometry, Western blotting, and transwell analyses. The target association was evaluated via dual-luciferase reporter analysis, RNA pull-down, and immunoprecipitation (RIP). Xenograft assay was performed using HCT116 cells. USP11 and Ki67 levels in tumor tissues were detected via immunohistochemistry. RESULTS: Circ_DOCK1 expression was enhanced in colorectal cancer tissues and cells. Silencing circ_DOCK1 repressed cell growth, migration, and invasion, and facilitated apoptosis. Circ_DOCK1 sponged miR-132-3p, and miR-132-3p silence mitigated the effect of circ_DOCK1 interference on cell growth, metastasis, and apoptosis. MiR-132-3p targeted USP11, and circ_DOCK1 could regulate USP11 level by miR-132-3p. MiR-132-3p suppressed cell growth, metastasis, and apoptosis, and USP11 attenuated these effects. Knockdown of circ_DOCK1 decreased colorectal cancer cell xenograft tumor growth. CONCLUSION: Circ_DOCK1 interference suppressed cell growth and metastasis, and increased apoptosis of colorectal cancer via decreasing USP11 by increasing miR-132-3p. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12957-021-02173-x. |
format | Online Article Text |
id | pubmed-7941900 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-79419002021-03-09 Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression Zhang, Weitong Wang, Zhenfen Cai, Guohao Huang, Ping World J Surg Oncol Research BACKGROUND: Circular RNAs (circRNAs) take part in colorectal cancer malignancies. CircRNA dedicator of cytokinesis 1 (circ_DOCK1) is involved in colorectal cancer progression, but the mechanism underlying this circRNA that takes part in colorectal cancer development remains largely undetermined. METHODS: Tumor and normal para-cancerous tissues were collected from 42 colorectal cancer patients. Human colorectal cancer cell lines (HCT116 and SW480) were used for the experiments in vitro. Circ_DOCK1, microRNA (miR)-132-3p, and ubiquitin-specific protease 11 (USP11) levels were measured through quantitative real-time polymerase chain reaction and Western blotting. Cell growth, metastasis, and apoptosis were investigated via colony formation, 5-ethynyl-2′-deoxyuridine (EdU) staining, MTT, flow cytometry, Western blotting, and transwell analyses. The target association was evaluated via dual-luciferase reporter analysis, RNA pull-down, and immunoprecipitation (RIP). Xenograft assay was performed using HCT116 cells. USP11 and Ki67 levels in tumor tissues were detected via immunohistochemistry. RESULTS: Circ_DOCK1 expression was enhanced in colorectal cancer tissues and cells. Silencing circ_DOCK1 repressed cell growth, migration, and invasion, and facilitated apoptosis. Circ_DOCK1 sponged miR-132-3p, and miR-132-3p silence mitigated the effect of circ_DOCK1 interference on cell growth, metastasis, and apoptosis. MiR-132-3p targeted USP11, and circ_DOCK1 could regulate USP11 level by miR-132-3p. MiR-132-3p suppressed cell growth, metastasis, and apoptosis, and USP11 attenuated these effects. Knockdown of circ_DOCK1 decreased colorectal cancer cell xenograft tumor growth. CONCLUSION: Circ_DOCK1 interference suppressed cell growth and metastasis, and increased apoptosis of colorectal cancer via decreasing USP11 by increasing miR-132-3p. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12957-021-02173-x. BioMed Central 2021-03-08 /pmc/articles/PMC7941900/ /pubmed/33685455 http://dx.doi.org/10.1186/s12957-021-02173-x Text en © The Author(s) 2021 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Zhang, Weitong Wang, Zhenfen Cai, Guohao Huang, Ping Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title | Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title_full | Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title_fullStr | Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title_full_unstemmed | Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title_short | Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression |
title_sort | circ_dock1 regulates usp11 through mir-132-3p to control colorectal cancer progression |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941900/ https://www.ncbi.nlm.nih.gov/pubmed/33685455 http://dx.doi.org/10.1186/s12957-021-02173-x |
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