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EIF4A3 induced circGRIK2 promotes the malignancy of glioma by regulating the miR-1303/HOXA10 axis.
Li, Fubin; Song, Wei; Wu, Lin; Liu, Bin; Du, Xinrui.
Afiliação
  • Li F; Department of Neurosurgery, Zibo Central Hospital Zibo 255036, Shandong, China.
  • Song W; Department of Breast and Thyroid Surgery, Zibo Central Hospital Zibo 255036, Shandong, China.
  • Wu L; Department of Pediatrics, Zhangdian Maternal and Child Health Care Hospital Zibo 255036, Shandong, China.
  • Liu B; Department of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University Jinan 250021, Shandong, China.
  • Du X; Department of Neurosurgery, Zibo Central Hospital Zibo 255036, Shandong, China.
Am J Cancer Res ; 13(12): 5868-5886, 2023.
Article em En | MEDLINE | ID: mdl-38187044
ABSTRACT
In recent years, the role of circular RNAs (circRNAs) in glioma has become increasingly important. However, there are still many newly discovered circRNAs with unknown functions that require further study. In this study, circRNA sequencing, qPCR, MTS, EdU, Transwell, and other assays were conducted to detect the expression and malignant effects of a novel circRNA molecule, circGRIK2, in glioma. qPCR, western blotting, RIP, and luciferase reporter gene experiments were used to investigate the downstream molecular mechanisms of circGRIK2. Our study found that circGRIK2 was highly expressed in glioma and promoted glioma cell viability, proliferation, invasion, and migration. Mechanistically, circGRIK2 acted as a competitive sponge for miR-1303, upregulating the expression of HOXA10 to exert its oncogenic effects. Additionally, the RNA-binding protein EIF4A3 could bind to and stabilize circGRIK2, leading to its high expression in glioblastoma. The discovery of circGRIK2 in this study not only contributes to a better understanding of the biological mechanisms of circGRIK2 in glioma but also provides a new target for molecular targeted therapy.
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Texto completo: 1 Bases de dados: MEDLINE Idioma: En Revista: Am J Cancer Res Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Bases de dados: MEDLINE Idioma: En Revista: Am J Cancer Res Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China