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A novel nanoplatform-based circCSNK1G3 affects CBX7 protein and promotes glioma cell growth.
Qiu, Cheng-Jie; Hu, Liang-Yun; Yang, Jin; Cao, Jiao-Jiao; Pei, Ben-Gen; Dai, Ran-Ran; Pan, Si-Jian.
Afiliação
  • Qiu CJ; Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao-Tong University, School of Medicine, Shanghai, China.
  • Hu LY; Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao-Tong University, School of Medicine, Shanghai, China.
  • Yang J; Department of Pulmonary and Critical Care Medicine, Rui-Jin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
  • Cao JJ; Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao-Tong University, School of Medicine, Shanghai, China.
  • Pei BG; Department of Neurosurgery, Zhou-Pu Hospital, Shanghai Jian-Kang University, School of Medicine, Shanghai, China. Electronic address: peibengen@163.com.
  • Dai RR; Department of Pulmonary and Critical Care Medicine, Rui-Jin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China. Electronic address: drr11154@rjh.com.cn.
  • Pan SJ; Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao-Tong University, School of Medicine, Shanghai, China. Electronic address: psj11629@rjh.com.cn.
Int J Biol Macromol ; 276(Pt 2): 134025, 2024 Sep.
Article em En | MEDLINE | ID: mdl-39033888
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: MicroRNAs / Proliferação de Células / Complexo Repressor Polycomb 1 / RNA Circular / Glioma Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: MicroRNAs / Proliferação de Células / Complexo Repressor Polycomb 1 / RNA Circular / Glioma Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article