Plk3, a member of the polo-like kinases (Plks) family, is a serine/threonine protein kinase. Plks are key regulators of the cell cycle, especially in the G2 phase and mitosis, and Plk3, along with Plk2, seems to have additional functions during G1, S, and G2 phases [2]. It is involved in multiple cellular processes such as the control of the cell cycle, apoptosis, and response to various stresses [3].

In cancer-related studies, high PLK3 expression was found to be associated with higher tumor stage and unfavorable prognosis in colorectal cancer patients, with a PLK3-positive rate ≥50% showing a strong correlation with shortened disease-free and overall survival [6]. In glioblastoma, PLK3 promoted the proneural-mesenchymal transition and tumor proliferation, and targeting it could decrease tumor growth and radioresistance [4]. In breast cancer, LINC00115 acts as a scaffold to link SETDB1 and PLK3, enhancing SETDB1 methylation of PLK3, which affects HIF1α stability and leads to chemoresistance and metastasis [1]. In renal ischemia-reperfusion injury, PLK3 was involved in oxidative stress-induced DNA damage and renal tubular epithelial cell apoptosis, and its inhibition attenuated apoptosis by blocking the ATM/P53-mediated DNA damage response [7]. In the context of influenza virus, PLK3 interacted with the viral nucleoprotein of swine influenza virus, promoting viral replication [5].

In conclusion, Plk3 is crucial in cell cycle regulation, stress response, and apoptosis. Its dysregulation is closely associated with various diseases, especially cancers. Studies on Plk3 using different models, though not specifically KO/CKO mouse models in the given references, have provided insights into its role in disease-related biological processes, which may help in developing therapeutic strategies for these diseases.