![Sample our Bioscience journals, sign in here to start your access, Latest two full volumes FREE to you for 14 days]({"type":"image" , "src" : "/sda/5925/TOC-Subject-Sample-2021-Bioscience.jpg"})
Abstract
Background
Previous research has revealed that activation or aberrant expression of kinases can lead to tumorigenesis of various cancers, including neuroblastoma (NB). Suppression of kinase expression can reduce drug resistance. We explored the potential role and mechanism of the aurora kinase B (AURKB) gene in the acquisition of carboplatin resistance in NB.
Methods
Immunohistochemistry (IHC) and qRT-PCR were used to explore the AURKB expression in NB patients. Subsequently, we structured Carboplatin-resistant NB cells. The potential biological functions of AURKB in carboplatin resistance were examined through knockdown of AURKB combined with CCK8, flow cytometry, immunohistochemistry, and western blot. Finally, overexpression of AURKB combined with ERK inhibitor (U0126) was carried out to explore the role of downstream signaling pathways.
Results
Overexpression of AURKB was closely correlated to poor prognosis in NB patients. In vitro, knockdown of AURKB could lead to a decline in IC50 value and restrain the invasion and the expression of MRP1 and Ki67, while promotes apoptosis in carboplatin-resistant cells (IMR-32-R and SK-N-AS-R). Additionally, AURKB overexpression could potentiate the invasion and the expression of MRP1 and Ki67, while suppresses apoptosis in SK-N-AS-R and IMR-32-R, whereas ERK inhibitor U0126 could reverse the phenomenon caused by AURKB overexpression.
Conclusion
AURKB overexpression was strongly associated with poor prognosis and carboplatin resistant acquisition. Additionally, suppression of AURKB-ERK axis might be a potential therapy for carboplatin resistance in NB patients.
Disclosure statement
No potential conflict of interest was reported by the author(s).