• Yuzhu Tang, Xiaohua Lan, Maohui Yan, Zhiguang Fu, and Hongqi Li.
• From the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.
• Saudi Med J. 2024 Feb 1; 45 (2): 128138128-138.

ObjectivesTo investigate the role of cell cycle protein-dependent kinase regulatory subunit 1B (CKS1B) in driving the aggressive and rapid proliferation observed in pancreatic cancer.MethodsA comprehensive analysis was carried out using raw mRNA information and data from 2 databases: the cancer genome atlas and gene expression omnibus. The differential expression of CKS1B at the mRNA and tissue levels in cancer and adjacent paracancerous tissues were assessed. Additionally, the relationship of CKS1B expression and overall survival (OS) rate was investigated using Kaplan-Meier survival curves. Potential molecular mechanisms by which CKS1B may influence the biological characteristics of pancreatic cancer were explored using resources available within the encyclopedia of RNA interactomes database.ResultsThe CKS1B exhibited significant differential expression at the mRNA as well as protein levels. A correlation with statistical significance between CKS1B expression and N stage, age, and alcohol consumption was observed. Notably, high CKS1B expression was determined as a predictive factor for worse OS. Furthermore, the analysis revealed a potential synergistic role between CKS1B and the molecule PKMYT1, which could impact the ATR-Chk1-Cdc25 signaling pathway and disrupt the G2/M checkpoint within the cell cycle, ultimately promoting abnormal tumor proliferation.ConclusionThe CKS1B may serve as a novel potential prognostic factor in pancreatic cancer and is involved in the abnormal proliferation biology phenotype by mediating cell cycle signaling pathways.Copyright: © Saudi Medical Journal.

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