Stk17b, also known as DRAK2, is a serine/threonine protein kinase belonging to the death-associated protein kinase family. It is involved in various biological processes such as setting the threshold for T cell activation, regulating Purkinje cell dendritic development, and is associated with pathways like AKT/GSK-3β/Snail. It has been genetically linked to the development of diverse diseases, making it an important gene for understanding disease mechanisms [4,5,7].

In cancer research, Stk17b has been found to be highly expressed in ovarian cancer, hepatocellular carcinoma, and glioma tissues, promoting tumor cell proliferation, invasion, and migration. For example, in ovarian cancer, silencing Stk17b suppressed cell progression, while overexpression promoted it, with Stk17b increasing cell invasion and migration by promoting the EMT process [1]. In hepatocellular carcinoma, inhibition of Stk17b inhibited tumorigenesis and metastasis, and it was found to promote the EMT process via the AKT/GSK-3β/Snail signal pathway [3]. In glioma, methionine deprivation-induced inhibition of Stk17b suppressed cell proliferation and the EMT process [6]. In skin cutaneous melanoma, Stk17b had lower expression compared to normal tissues, and its low expression was correlated with poor overall survival and disease-specific survival, and it was also related to immune infiltration [2].

In conclusion, Stk17b plays a crucial role in multiple biological processes and disease conditions, especially in cancer progression. Its role in promoting tumorigenesis and metastasis in various cancers, as well as its association with immune-related processes in skin cutaneous melanoma, makes it a potential target for cancer diagnosis, prognosis, and immunotherapy. The findings from these functional studies help in understanding the complex mechanisms underlying these diseases and may lead to the development of novel therapeutic strategies.