EMP1 correlated with cancer progression and immune characteristics in pan-cancer and ovarian cancer

Mol Genet Genomics. 2024 May 14;299(1):51. doi: 10.1007/s00438-024-02146-1.

Abstract

This study examines the prognostic role and immunological relevance of EMP1 (epithelial membrane protein-1) in a pan-cancer analysis, with a focus on ovarian cancer. Utilizing data from TCGA, CCLE, and GTEx databases, we assessed EMP1 mRNA expression and its correlation with tumor progression, prognosis, and immune microenvironment across various cancers. Our results indicate that EMP1 expression is significantly associated with poor prognosis in multiple cancer types, including ovarian, bladder, testicular, pancreatic, breast, brain, and uveal melanoma. Immune-related analyses reveal a positive correlation between EMP1 and immune cell infiltration, particularly neutrophils, macrophages, and dendritic cells, as well as high expression of immune checkpoint such as CD274, HAVCR2, IL10, PDCD1LG2, and TGFB1 in most tumors. In vivo experiments confirm that EMP1 promotes ovarian cancer cell proliferation, metastasis, and invasion. In conclusion, EMP1 emerges as a potential prognostic biomarker and therapeutic target in various cancers, particularly ovarian cancer, due to its influence on tumor progression and immune cell dynamics. Further research is warranted to elucidate the precise mechanisms of EMP1 in cancer biology and to translate these findings into clinical applications.

Keywords: EMP1; Immune infiltration; Ovarian cancer; Pan-cancer; The Cancer Genome Atlas.

MeSH terms

  • Animals
  • Biomarkers, Tumor* / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Disease Progression*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Membrane Glycoproteins / genetics
  • Mice
  • Neoplasms / genetics
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Ovarian Neoplasms* / genetics
  • Ovarian Neoplasms* / immunology
  • Ovarian Neoplasms* / pathology
  • Prognosis
  • Tumor Microenvironment* / genetics
  • Tumor Microenvironment* / immunology