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Inhibition of BUB1 suppresses tumorigenesis of osteosarcoma via blocking of PI3K/Akt and ERK pathways.

Authors :
Huang, Zhen
Wang, Shenglin
Wei, Hongxiang
Chen, Hui
Shen, Rongkai
Lin, Renqin
Wang, Xinwen
Lan, Wenbin
Lin, Rongjin
Lin, Jianhua
Source :
Journal of Cellular & Molecular Medicine; Sep2021, Vol. 25 Issue 17, p8442-8453, 12p
Publication Year :
2021

Abstract

Osteosarcoma (OS) is a primary malignant bone tumour that mainly affects teenagers, with patients displaying poor prognosis. Budding uninhibited by benzimidazoles 1 (BUB1), a type of serine/threonine kinase that is linked to pro‐tumorigenic phenomena, has not been well studied in OS. Hence, this study aimed to explore the role of BUB1 in OS. The expression of BUB1 in OS specimens and cell lines was assessed using immunohistochemistry and Western blot analysis. Univariate and multivariate analyses were applied to evaluate the impact of BUB1 on patient survival. Cell counting kit‐8, wound‐healing and Transwell assays, as well as flow cytometry, were used to investigate the influence of BUB1 inhibition on OS in vitro. Moreover, a tumour xenograft model was established to investigate the in vivo effect of BUB1 inhibition on OS tumour growth. Results showed that BUB1 was overexpressed in OS specimens and cell lines. Furthermore, BUB1 overexpression was closely associated with the poor clinical outcomes of patients with OS. Inhibition of BUB1 markedly suppressed cell proliferation and tumour growth, cell migration, invasion and induced cell apoptosis of OS by blocking the PI3K/Akt and ERK signalling pathways. Thus, our study suggested that overexpression of BUB1 protein contributed to poor survival of OS patients and that inhibition of BUB1 resulted in considerable anti‐tumour activity associated with proliferation, migration, invasion and apoptosis of OS. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15821838
Volume :
25
Issue :
17
Database :
Complementary Index
Journal :
Journal of Cellular & Molecular Medicine
Publication Type :
Academic Journal
Accession number :
152290948
Full Text :
https://doi.org/10.1111/jcmm.16805