Purpose: Our purpose was to systematically appraise the clinicopathological significance and explore the molecular bases of CKS2 in
endometrial carcinoma. Patients and Methods: We measured the clinicopathological significance of CKS2 using diverse methods of public
RNA-seq, microarrays, and in-house tissue microarrays to investigate the molecular basis of CKS2 in
endometrial carcinoma through upstream transcriptional analysis, immune infiltration correlation analysis, and co-expression analysis. Results: Both the analysis for public
RNA-seq plus the microarray data and in-house tissue microarray confirmed the significant overexpression of CKS2 in a total of 1,021
endometrial carcinoma samples compared with 279 non-
cancer endometrium samples (SMD = 2.10, 95% CI = 0.72-3.48). The upregulated CKS2 was significantly related to the
lymph node metastasis and advanced clinical grade of
endometrial carcinoma patients (p < 0.001). Mutation types such as amplification and
mRNA occurred with high frequency in the CKS2 gene in
endometrial carcinoma patients. A series of
miRNAs and
transcription factors, such as hsa-miR-26a, hsa-miR-130a, hsa-miR-30, E2F4, MAX, and GABPA, were predicted to regulate the transcription and expression of CKS2. Significant links were found between CKS2 expression and the infiltration level of B cells, CD4+ T cells, and neutrophils in
endometrial carcinoma. CKS2-coexpressed genes were actively involved in pathways such as the mitotic cell cycle process, PID aurora B pathway, and
prolactin signaling pathway. Conclusion: The overexpressed CKS2 showed positive correlations with the
clinical progression of
endometrial carcinoma and was associated with various
cancer-related biological processes and pathways, showing potential as a promising clinical
biomarker for
endometrial carcinoma.