Cks2, also known as cyclin-dependent kinase subunit 2 or CDC28 protein kinase regulatory subunit 2, is involved in cell cycle and proliferation processes [2,3,6]. It is associated with multiple biological pathways, potentially regulating certain important genes. Given its role in cell-related processes, genetic models such as gene knockout or conditional knockout mouse models could be valuable for in-depth functional studies.

In various cancers, Cks2 shows abnormal expression. In colon cancer, knockdown of Cks2 enhances Erastin-induced ferroptosis by reducing glutathione (GSH) metabolism, while overexpression has the opposite effect, as Cks2-induced autophagy reinforces GSH metabolism to increase ferroptosis resistance [1]. In pediatric retinoblastoma, depletion of Cks2 in cell lines leads to reduced cell proliferation, delayed DNA replication, decreased clonogenic growth, and slowed tumor xenograft growth in nude mice [3]. In non-small-cell lung cancer, knockdown of Cks2 suppresses cell viability, foci formation, and tumorigenesis in vivo [4]. In glioma, Cks2 knockdown impedes the expansion and aggression of glioma cell lines [5].

In conclusion, Cks2 plays a crucial role in cell cycle and proliferation. Its abnormal expression is closely associated with the development and progression of multiple cancers, including colon cancer, retinoblastoma, non-small-cell lung cancer, and glioma. Studies using gene-knockout or knockdown models in these cancer types have revealed its role in promoting tumor growth, cell survival, and resistance to cell death mechanisms like ferroptosis, highlighting its potential as a therapeutic target for these diseases.