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Coronin 3 Promotes the Development of Oncogenic Properties in Glioma Through the Wnt/β-Catenin Signaling Pathway
- Source :
- OncoTargets and Therapy. 13:6661-6673
- Publication Year :
- 2020
- Publisher :
- Informa UK Limited, 2020.
-
Abstract
- Purpose Evidence indicates that the actin-binding protein Coronin 3, which is aberrantly expressed in various cancers, is associated with cancer development and progression. However, little is known about the role of Coronin 3 in glioma tumorigenesis. Here, we aimed to explore the biological function and regulatory mechanism of Coronin 3 in glioblastoma (GBM). Materials and methods Coronin 3 level in human GBM clinical samples and cell lines was investigated. The shRNA knockdown strategy was used to assess the tumor characteristics of GBM cell lines. The role of β-catenin in Coronin 3-mediated oncogenic phenotypes was evaluated. Results Coronin 3 was found to be highly upregulated in glioma cell lines. Furthermore, knockdown of Coronin 3 significantly inhibited the growth of glioma cells both in vivo and in vitro and suppressed the expression of Wnt/β-catenin pathway genes, including β-catenin, Cyclin D1, and c-Myc. Moreover, we demonstrated that Coronin 3 regulates the expression of β-catenin in glioma. Our results revealed that Coronin 3-stimulated tumor growth was β-catenin-dependent. Conclusion Our study reveals a new molecular mechanism of Coronin 3 in promoting glioma growth and development through regulating the Wnt/β-catenin signaling pathway.
- Subjects :
- 0301 basic medicine
Gene knockdown
biology
Wnt signaling pathway
Coronin
medicine.disease_cause
medicine.disease
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
Cyclin D1
Oncology
Downregulation and upregulation
030220 oncology & carcinogenesis
Glioma
medicine
Cancer research
biology.protein
Pharmacology (medical)
Signal transduction
Carcinogenesis
Subjects
Details
- ISSN :
- 11786930
- Volume :
- 13
- Database :
- OpenAIRE
- Journal :
- OncoTargets and Therapy
- Accession number :
- edsair.doi...........21f78ebf8fcd740da4fe6c4c9c75823b