학술논문
Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHDI
ORIGINAL RESEARCH
ORIGINAL RESEARCH
Document Type
Academic Journal
Source
Cancer Management and Research. October 31, 2020, Vol. 12, p10055, 11 p.
Subject
Language
English
ISSN
1179-1322
Abstract
Introduction Glioma is the most common brain tumor with low 5-year overall survival. (1) Great advances have gained on understanding the biology of glioma because of the development of experimental [...]
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 (CHDI) 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. Keywords: glioma, circ-TTBK2, miR-1283, CHD1, migration, glycolysis
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 (CHDI) 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. Keywords: glioma, circ-TTBK2, miR-1283, CHD1, migration, glycolysis