
-   Higher expression of CDK1 was associated with poorer prognosis in hepatocellular carcinoma (HCC) patients. Lower promoter methylation of this gene might cause higher expression levels in tumor tissues of HCC. Several methylated-CpG sites in this gene were significantly associated with survival. Notably, expression levels of CDK1 was positively correlated with infiltrating levels of CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells in HCC [PMID: 32863381]. CDK1 knockdown suppressed the expression of PLK1, ANLN, and SGOL2. The CDK1-PLK1/SGOL2/ANLN pathway mediating abnormal cell division in the cell cycle might be a critical process in hepatocellular carcinoma (HCC) [PMID: 32275843].

## Summary

CDK1, coded by the Cdk1 gene, is a Ser/Thr protein kinase that serves as a catalytic subunit in the M-phase promoting factor complex, instrumental for G2/M phase transitions within the cell cycle [CS: 10]. Its activity, regulated through interactions with cyclins and controlled phosphorylation-dephosphorylation events, is essential for progressions such as centrosome separation [CS: 10], Golgi dynamics [CS: 8], nuclear envelope breakdown [CS: 10], chromosome condensation [CS: 10], later chromosome decondensation [CS: 9], reformation of the nuclear envelope [CS: 9], and cytokinesis [CS: 10]. In diseases such as autosomal dominant polycystic kidney disease (ADPKD), CDK1's dysregulation manifests as a disturbance in cell cycle control and a driver of cell proliferation [CS: 8], with evidence detailing aberrant expression levels contributing to these pathologies [CS: 8].

In the context of kidney toxicities and diseases, dysregulation of CDK1 gene expression may be a direct response to the toxic events triggering cellular stress and damage, prompting a compensatory mechanism aimed at survival [CS: 7]. For instance, in renal cell carcinoma cells, upregulation of RhoB leads to aberrant expression of CDK1 and other cycle regulators, implicating CDK1 in tumor proliferation and resistance to apoptosis [CS: 8]. In autosomal dominant polycystic kidney disease models, Cdk1 dysregulation is noted prior to cyst formation, with its role as an early facilitator of cell proliferation suggesting an attempt to counteract initial renal damage [CS: 8]. Similarly, in diabetic nephropathy, increased CDK1 expression in the presence of hyperglycemia could be indicative of kidney cells striving to overcome glucotoxicity-driven damage through escalated cell cycle activity and tissue regeneration [CS: 6]. These alterations in CDK1 expression reinforce its significance not only in cell cycle progression but also in pathological conditions where its regulation can influence disease outcomes, such as promoting cell survival and continued proliferation in the face of renal impairments [CS: 7].
