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Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1
BACKGROUND: Dysregulated circular RNAs (circRNAs) are involved in the development of glioma. This paper aims to analyze the role and mechanism of circRNA tau tubulin kinase 2 (circ-TTBK2) in glioma progression. METHODS: The glioma samples and normal brain tissues were collected. The levels of circ-T...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568596/ https://www.ncbi.nlm.nih.gov/pubmed/33116862 http://dx.doi.org/10.2147/CMAR.S252916 |
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author | Han, Chengchen Wang, Shuwei Wang, Hongwei Zhang, Jianning |
author_facet | Han, Chengchen Wang, Shuwei Wang, Hongwei Zhang, Jianning |
author_sort | Han, Chengchen |
collection | PubMed |
description | BACKGROUND: Dysregulated circular RNAs (circRNAs) are involved in the development of glioma. This paper aims to analyze the role and mechanism of circRNA tau tubulin kinase 2 (circ-TTBK2) in glioma progression. METHODS: The glioma samples and normal brain tissues were collected. The levels of circ-TTBK2, microRNA-1283 (miR-1283) and chromodomain helicase DNA-binding protein 1 (CHD1) were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Cell proliferation, migration, invasion and glycolysis were determined via 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, transwell assay, Western blot, glucose and lactate assay kits. The target relationship was analyzed via dual-luciferase reporter assay. The xenograft model was established using U251 cells. RESULTS: circ-TTBK2 expression was increased in glioma tissues and cells. circ-TTBK2 knockdown suppressed glioma cell proliferation, migration, invasion and glycolysis. circ-TTBK2 was a sponge for miR-1283, and knockdown of miR-1283 reversed the effect of circ-TTBK2 silence on glioma progression. CHD1 was targeted via miR-1283, and miR-1283 repressed glioma cell proliferation, migration, invasion and glycolysis via decreasing CHD1. Knockdown of circ-TTBK2-reduced CHD1 expression by mediating miR-1283. Silence of circ-TTBK2 reduced xenograft tumor growth. CONCLUSION: Down-regulation of circ-TTBK2 suppressed glioma development by regulating miR-1283 and CHD1, providing a new mechanism for understanding glioma pathogenesis. |
format | Online Article Text |
id | pubmed-7568596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-75685962020-10-27 Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 Han, Chengchen Wang, Shuwei Wang, Hongwei Zhang, Jianning Cancer Manag Res Original Research BACKGROUND: Dysregulated circular RNAs (circRNAs) are involved in the development of glioma. This paper aims to analyze the role and mechanism of circRNA tau tubulin kinase 2 (circ-TTBK2) in glioma progression. METHODS: The glioma samples and normal brain tissues were collected. The levels of circ-TTBK2, microRNA-1283 (miR-1283) and chromodomain helicase DNA-binding protein 1 (CHD1) were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Cell proliferation, migration, invasion and glycolysis were determined via 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, transwell assay, Western blot, glucose and lactate assay kits. The target relationship was analyzed via dual-luciferase reporter assay. The xenograft model was established using U251 cells. RESULTS: circ-TTBK2 expression was increased in glioma tissues and cells. circ-TTBK2 knockdown suppressed glioma cell proliferation, migration, invasion and glycolysis. circ-TTBK2 was a sponge for miR-1283, and knockdown of miR-1283 reversed the effect of circ-TTBK2 silence on glioma progression. CHD1 was targeted via miR-1283, and miR-1283 repressed glioma cell proliferation, migration, invasion and glycolysis via decreasing CHD1. Knockdown of circ-TTBK2-reduced CHD1 expression by mediating miR-1283. Silence of circ-TTBK2 reduced xenograft tumor growth. CONCLUSION: Down-regulation of circ-TTBK2 suppressed glioma development by regulating miR-1283 and CHD1, providing a new mechanism for understanding glioma pathogenesis. Dove 2020-10-13 /pmc/articles/PMC7568596/ /pubmed/33116862 http://dx.doi.org/10.2147/CMAR.S252916 Text en © 2020 Han et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Han, Chengchen Wang, Shuwei Wang, Hongwei Zhang, Jianning Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title | Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title_full | Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title_fullStr | Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title_full_unstemmed | Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title_short | Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1 |
title_sort | knockdown of circ-ttbk2 inhibits glioma progression by regulating mir-1283 and chd1 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568596/ https://www.ncbi.nlm.nih.gov/pubmed/33116862 http://dx.doi.org/10.2147/CMAR.S252916 |
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