Ccnk, also known as cyclin K, is a regulator of transcription thought to play a critical role in RNA polymerase II-mediated activities. It forms a complex with CDK12 and is potentially involved in pre-mRNA cleavage and polyadenylation [3,4].

In Ccnk-related syndrome, both patient-derived neural progenitor cells (NPCs) and Ccnk knockout (KO) mouse models showed deficient NPC proliferation and enhanced apoptotic cell death. RNA sequencing of these NPC models revealed significant changes in genes like WNT5A, which is crucial for progenitor proliferation and cell death. A Wnt5a inhibitor increased proliferation and reduced apoptosis in NPCs from patients with CCNK-related syndrome and in NPCs in the developing cortex of Ccnk KO mice, indicating that CCNK plays critical roles in NPC proliferation and apoptosis in vivo and in vitro [1]. In colorectal cancer, knockout of CCNK decreased the proliferation of CRC cells in vitro and tumor growth in vivo, suggesting that CCNK is involved in the growth of this cancer type [2].

In conclusion, Ccnk is important for transcription-related processes and pre-mRNA processing. The Ccnk KO mouse models have revealed its role in neural progenitor cell regulation in Ccnk-related syndrome, highlighting its significance in neurodevelopmental disorders. In addition, its role in colorectal cancer growth also indicates its potential importance in cancer research.