SBK1, also known as SH3 domain binding kinase 1, is a serine/threonine kinase belonging to the new kinase family (NFK). It has been implicated in various biological processes such as memory formation, lipid metabolism, and cancer cell progression [1]. It may be involved in multiple signaling pathways, and its expression is regulated by hormones and nutrients [1].

In terms of lipid metabolism, SBK1 is a regulator of hepatic lipid metabolism and systemic insulin sensitivity in response to obesity. Liver-specific SBK1 knockout (Lsko) mice fed a high-fat diet (HFD) displayed more severe hepatosteatosis, higher expression of genes in fatty acid uptake and lipogenesis, symptoms of hyperglycemia, poor systemic glucose tolerance, and lower insulin sensitivity compared to control mice. On the other hand, hepatic SBK1 overexpression alleviated high-fructose diet-induced hepatosteatosis, hyperlipidemia, and hyperglycemia in mice [2].

In cancer, in cervical cancer, SBK1 promotes proliferation and inhibits apoptosis via activating the Wnt/β-catenin and Raf/ERK1/2 signaling pathways. Stable SBK1-knockdown in cervical cancer cells suppressed their proliferative, migratory, and invasive capacities and enhanced apoptosis [3].

In conclusion, SBK1 plays a crucial role in lipid metabolism, protecting against hepatic steatosis and insulin resistance through the Nur77-FGF21 pathway. In cancer, it can promote cancer cell survival and proliferation in certain types such as cervical cancer. The use of gene knockout mouse models, like the liver-specific SBK1 knockout mice, has been instrumental in revealing its functions in these biological processes and disease conditions.