1. A novel nanoplatform-based circCSNK1G3 affects CBX7 protein and promotes glioma cell growth.
- Author
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Qiu CJ, Hu LY, Yang J, Cao JJ, Pei BG, Dai RR, and Pan SJ
- Subjects
- Humans, Animals, Cell Line, Tumor, Mice, Gene Expression Regulation, Neoplastic, Brain Neoplasms genetics, Brain Neoplasms metabolism, Brain Neoplasms pathology, Mice, Nude, Dependovirus genetics, Glioma genetics, Glioma metabolism, Glioma pathology, MicroRNAs genetics, MicroRNAs metabolism, Cell Proliferation, RNA, Circular genetics, RNA, Circular metabolism, Polycomb Repressive Complex 1 genetics, Polycomb Repressive Complex 1 metabolism
- Abstract
Bioenvironmental and biological factors have the potential to contribute to the development of glioma, a type of brain tumor. Recent studies have suggested that a unique circular RNA called circCSNK1G3 could play a role in promoting the growth of glioma cells. It does this by stabilizing a specific microRNA called miR-181 and reducing the expression of a tumor-suppressor gene known as chromobox protein homolog 7 (CBX7). To further investigate circCSNK1G3 and its effects on glioma, we utilized a nanoplatform called adeno-associated virus (AAV)-RNAi.To explore the functional implications of circCSNK1G3, we employed siRNA to silence its expression. Along with these effects, the silencing of circCSNK1G3 led to a depletion of miR-181d and an upregulation of CBX7. When we introduced miR-181d mimics, which artificially increase the levels of miR-181d, the anti-glioma cell activity induced by circCSNK1G3 siRNA was almost completely reversed. Conversely, inhibiting miR-181d mimicked the effects of circCSNK1G3 silencing. Moreover, when we overexpressed circCSNK1G3 in glioma cells, we observed an elevation of miR-181d and a depletion of CBX7. We found that the growth of A172 xenografts (tumors) carrying circCSNK1G3 shRNA was significantly inhibited. In these xenograft tissues, we detected a depletion of circCSNK1G3 and miR-181d, as well as an upregulation of CBX7., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)
- Published
- 2024
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