Cdk1, short for cyclin-dependent kinase 1, is a crucial regulator in the cell cycle. It forms complexes with cyclins, especially cyclin B1, and plays a central role in driving cells through the G2/M phase transition. This process is fundamental for cell division and normal tissue development and maintenance. Cdk1-mediated regulation is also involved in multiple cellular pathways, such as those related to energy metabolism, autophagy, and gene regulation [2,4].

In cancer research, genetic and pharmacological blockade of Cdk1 has shown promising results. In colorectal cancer, CDK1 was identified as a contributor to oxaliplatin resistance. Blocking CDK1 restored the susceptibility of CRC cells to oxaliplatin in vitro and in xenograft models by regulating ACSL4-mediated ferroptosis [1]. In triple-negative breast cancer, CDK1 phosphorylates USP29, stabilizing TWIST1 and promoting chemo-resistance and metastasis, and its inhibition could mitigate these phenotypes [3]. In adrenocortical carcinoma, overexpression of CDK1 promoted cell proliferation and epithelial-to-mesenchymal transition, while its inhibitor cucurbitacin E showed good anti-tumor effects both in vitro and in vivo [5].

In conclusion, Cdk1 is essential for cell cycle progression and is involved in multiple cellular functions. Through genetic models like gene knockout or pharmacological inhibition, research has revealed its significant role in cancer drug resistance, tumor progression, and metastasis. Targeting Cdk1 could be a potential therapeutic strategy for treating various cancers, highlighting the importance of Cdk1-related research in oncology.