Bioinformatics approaches to multi-omics analysis of the potential of CDKN2A as a biomarker and therapeutic target for uterine corpus endometrial carcinoma

Sci Rep. 2025 Jan 6;15(1):895. doi: 10.1038/s41598-025-85364-w.

Abstract

Uterine corpus endometrial carcinoma (UCEC) is a significant cause of cancer-related mortality among women worldwide. Prior research has demonstrated an association between cyclin-dependent kinase inhibitor 2 A (CDKN2A) and various tumors. As a member of the INK4 family, CDKN2A is involved in cell cycle regulation by controlling CDKs. In the present study, bioinformatics was used to analyze public datasets. The expression levels, signaling pathways, and copy number variations of CDKN2A in UCEC were explored, along with its immune cell subset associations. CDKN2A expression was found to be elevated in UCEC, particularly in the signaling pathways involved in cell proliferation and inflammation. Analysis of somatic copy number alterations in the TCGA (The Cancer Genome Atlas)-UCEC dataset revealed a connection between CDKN2A and drug metabolism in UCEC. Assessment of the relationship between CDKN2A and genes involved in immunotherapy for UCEC patients showed a negative correlation between CDKN2A and CD8+ T cell activity, as well as IL-2 and TP53. Collectively, these insights suggest that CDKN2A may be a potential biomarker for prognosis and treatment strategies in UCEC.

Keywords: CDKN2A; CDKN2A expression; Immunotherapy; Somatic copy number alteration analysis; Uterine corpus endometrial carcinoma.

MeSH terms

  • Biomarkers, Tumor* / genetics
  • Biomarkers, Tumor* / metabolism
  • CD8-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / metabolism
  • Computational Biology* / methods
  • Cyclin-Dependent Kinase Inhibitor p16* / genetics
  • Cyclin-Dependent Kinase Inhibitor p16* / metabolism
  • DNA Copy Number Variations
  • Endometrial Neoplasms* / genetics
  • Endometrial Neoplasms* / metabolism
  • Endometrial Neoplasms* / pathology
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Interleukin-2 / genetics
  • Interleukin-2 / metabolism
  • Multiomics
  • Prognosis
  • Signal Transduction
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • Biomarkers, Tumor
  • CDKN2A protein, human
  • Tumor Suppressor Protein p53
  • Interleukin-2