Cks1b, Cyclin-dependent kinase regulatory subunit 1B, is a member of the conserved cyclin kinase subunit 1 (CKS1) protein family. It plays an essential role in cell cycling and is involved in multiple signaling pathways, such as JAK/STAT3, MEK/ERK, and the cell cycle-related ATR-Chk1-Cdc25 pathway. Its biological importance extends to cancer pathogenesis and the regulation of cardiomyocyte proliferation-maturation transition [1,2].

In cancer research, loss-of-function experiments have been revealing. For example, knockdown of Cks1b in hepatocellular carcinoma cell lines inhibited cell survival, proliferation, migration, invasion, and induced apoptosis, and it was shown to do so by inhibiting the JAK/STAT3 pathway [3]. In retinoblastoma cells, shRNA-mediated downregulation of Cks1b restrained cell proliferation, migration, invasion, and angiogenesis through suppressing the MEK/ERK signaling pathway [6]. In pancreatic cancer, Cks1b knockdown reduced cell viability and invasion, and also sensitized cells to gemcitabine and oxaliplatin treatment [4,5].

In conclusion, Cks1b is crucial for normal cell cycling and its dysregulation is implicated in various cancers. The gene knockout or knockdown models have demonstrated its oncogenic role in promoting cancer cell proliferation, migration, and invasion, as well as its association with drug resistance. These findings suggest that Cks1b could be a potential therapeutic target for cancer treatment [1,3-8].