SBK1 (SH3 Domain Binding Kinase 1)

Expression pattern alterations of prognostic genes were observed in endothelial cells, T cells, and epithelial cells. In conclusion, a risk model based on mitophagy- and MD-related prognostic genes was established, offering a promising approach for the personalized management of patients with CC.

Meanwhile, the expression of the Notch signaling pathway-related proteins was downregulated after E2F1 knockdown and could also be restored by SBK1 overexpression. This study elucidated the mechanism of SBK1/E2F1 involved in the progression of breast cancer and provided a new target for the treatment of breast cancer.

Mechanistic analysis showed that SBK1 is under the DRAIC competing endogenous RNAs network, potentially through sponging of miRNA-92a. Consistent dysregulation of the DRAIC-SBK1 axis was linked to poor survival outcome in both LUAD and LUSC, suggesting a tumour inhibitor role and providing potential for new diagnostics and therapeutic approaches.

In contrast, insulin had a differential action on SBK1 expression that it promoted the expression of all SBK1 isoforms in the goldfish hepatocytes but inhibited Sbk1 expression in the mouse hepatocytes. Together, our findings indicate that SBK1 expression is hormone- and nutrient-sensitive with a species-specific response.

FBP1, SBK1, and AURKA are prognostic risk factors, and the risk model and nomogram of FBP1, SBK1 and AURKA are associated with dismal prognosis and immune cell infiltration, and have huge prospects for application in evaluating the prognosis in LUAD.

SBK1 overexpression also contributed to tumor growth in vivo. Overall, SBK1 played a vital role in cervical tumorigenesis via activating the Wnt/β-catenin and Raf/ERK1/2 pathways.