A novel circular RNA, hsa{sub c}irc{sub 0}046701, promotes carcinogenesis by increasing the expression of miR-142-3p target ITGB8 in glioma
- Department of Neurosurgery, The Affiliated Hospital of Qingdao University (China)
- Department of Anesthesiology, The Affiliated Hospital of Qingdao University (China)
Highlights: • We identified a novel circular RNA, hsa{sub c}irc{sub 0}046701 in glioma cells. • Hsa{sub c}irc{sub 0}046701 was significantly upregulated in glioma tissues. • Hsa{sub c}irc{sub 0}046701 sponges miR-142-3p in glioma. • MiR-142-3p directly targets ITGB8 in glioma. • Hsa{sub c}irc{sub 0}046701/miR-142-3p/ITGB8 axis plays critical roles in glioma pathogenesis. In the present study, we identified a novel circular RNA (circRNA), hsa{sub c}irc{sub 0}046701, in glioma cells. We measured the expression of hsa{sub c}irc{sub 0}046701 using qRT-PCR in glioma tissues and cell lines, and explored its functions using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, and Transwell assays. Luciferase reporter assays were performed to validate the correlation between microRNA miR-142-3p and hsa{sub c}irc{sub 0}046701 or integrin subunit beta 8 (ITGB8). The results showed that hsa{sub c}irc{sub 0}046701 was significantly upregulated in glioma tissues and cell lines, and knockdown of hsa{sub c}irc{sub 0}046701 inhibited cell proliferation and invasion. Luciferase reporter assays indicated that hsa{sub c}irc{sub 0}046701 functions as a sponge for miR-142-3p and regulates the expression of ITGB8. Subsequently, functional assays revealed that silencing of hsa{sub c}irc{sub 0}046701 could upregulate miR-142-3p, resulting in downregulation of ITGB8. The results demonstrated that the hsa{sub c}irc{sub 0}046701/miR-142-3p/ITGB8 axis might play critical regulatory roles in the pathogenesis and development of glioma.
- OSTI ID:
- 23137256
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 498, Issue 1; Other Information: Copyright (c) 2018 Published by Elsevier Inc.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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