Identification of CKS2 as a novel prognostic biomarker and potential therapeutic target for oral squamous cell carcinoma

Abstract

Background The cyclin-dependent kinase subunit 2 ( CKS2 ) is recognized to have a substantial impact on the pathogenesis and advancement of several malignant neoplasms. Nevertheless, its biological function and prognostic significance in oral squamous cell carcinoma (OSCC) have yet to be thoroughly investigated. Our primary objective was to clarify the contribution of CKS2 in the progression and prognosis of OSCC. Methods We first conducted a thorough examination of online databases to investigate the expression of CKS2 , and subsequently corroborated our discoveries by analyzing clinical specimens that we collected. According to the clinicopathological data, we then explored the prognostic significance of CKS2 . Furthermore, we predicted the role of CKS2 in OSCC progression by employing weighted gene co-expression network analysis (WGCNA) in conjunction with functional enrichment analysis. We conducted functional experiments in vitro to confirm our speculations. Additionally, we explored other potential functions of CKS2 in immune infiltration, tumor mutation burden (TMB), and drug sensitivity. Finally, we established and validated a nomogram that effectively integrated CKS2 -related genes and other relevant clinical factors. Results Our findings indicated a significant upregulation of CKS2 expression in OSCC tissues compared to normal groups, which was positively associated with poor clinical outcomes. We also predicted and validated the role of CKS2 in promoting proliferation by regulating the cell cycle. Additionally, its upregulation was significantly correlated to enhanced immune cell infiltration, high TMB, and increased sensitivity of anti-tumor agents. Following verification, the nomogram was conducted to quantify an individual’s survival probability. Conclusions In general, our study indicates that CKS2 is a novel prognostic biomarker and potential therapeutic target in OSCC.