Aurora kinase inhibition downregulates NF-κB and sensitises tumour cells to chemotherapeutic agents

Retracted: Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV‐1‐infected T cells through enhanced NF‐κB activity

“…26 In this regard, inhibition of Aurora kinases was reported to downregulate NF-jB activity and to enhance the efficacy of cytotoxic drugs on lung and ovarian cancer cell lines. 27 However direct target of Aurora A have not been identified in NF-jB signaling molecules. In this study, we found that Aurora A activated Tax-induced NF-jB reporter activity, however without Tax it could not activate NF-jB reporter (Fig.…”

“…25 Recent studies have suggested that Aurora A activates NF-jB signaling pathway in some cancer cell lines. 26,27 In this study, we investigated the effects of Aurora A on the growth and survival of HTLV-1-infected T-cell lines and primary ATL cells, with a special focus on NF-jB signaling pathway.…”

USP7 and Daxx regulate mitosis progression and taxane sensitivity by affecting stability of Aurora-A kinase

“…Use of these drugs has been shown to sensitize Aurora-A-overexpressing tumor cells to chemotherapeutic agents including taxanes. 45 Thus, we next tested whether Aurora-A inhibition could over-ride USP7-mediated Taxol resistance. MLN8054 was tested alone or in combination with Taxol, in cells stably expressing control or USP7 shRNAs (Figure 6b).…”

Aurora kinase inhibitor VE 465 synergistically enhances cytotoxicity of carboplatin in ovarian cancer cells through induction of apoptosis and downregulation of histone 3

“…6 Ectopic overexpression of Aurora kinases in mammalian cells induces centrosome amplification, 7 chromosome instability, 8 oncogenic transformation 8 and chemoresistance. 9 Overexpression of Aurora kinases has been detected in a wide range of human tumors, 10,11 including aurora kinases are essential for regulation of chromosome segregation and cytokinesis during mitosis and play a role in growth and progression of human tumors, including ovarian cancer. aurora a and aurora B are frequently overexpressed in high-grade and low-grade ovarian cancers.…”

“…9,32,33 It has also been suggested that Aurora A activates Akt and induces cell survival and chemoresistance in a p53-dependent 32 μg/mL, while it was slightly reduced by the combination of carboplatin with 1 μM VE 465. This result was consistent with the finding that phosphorylated H3 expression was significantly reduced by VE 465 alone and by co-treatment with VE 465 and carboplatin, suggesting that the growth-inhibitory effect of combined treatment on ovarian cancer cell lines was associated with inhibition of Aurora B activity (Fig.…”