Activin levels correlate with lymphocytic infiltration in epithelial ovarian cancer

Cancer Med. 2024 Sep;13(17):e7368. doi: 10.1002/cam4.7368.

Abstract

Objective: The TGF-β superfamily member activin, a dimer of the gene products of INHBA and/or INHBB, has been implicated in immune cell maturation and recruitment, but its immune impact within epithelial ovarian cancer (EOC) is not well characterized. We sought to explore differences in activin (INHBA/ Inhibin-βA and INHBB/ Inhibin-βB) between malignant and ovarian tissues at the RNA and protein level and assess the relationship between activin and immune cells in EOC.

Methods: Publicly available RNA sequencing data were accessed from GEO (#GSE143897) with normalization and quantification performed via DESeq2. Immune gene expression profile was further explored within the TCGA-OV cohort derived from The Cancer Genome Atlas (TCGA). Immunohistochemical analysis was performed to evaluate activin A and T-cell markers CD8 and FoxP3 at the protein level. ELISA to activin-A was used to assess levels in the ascites of advanced EOC patients. Kaplan-Meier curves were generated to visualize survival outcomes.

Results: Gene expression levels of components of the activin signaling pathway were elevated within EOC when compared to a benign cohort, with differences in activin type I/II receptor gene profiles identified. Additionally, INHBA gene expression was linked to lymphocytic immune markers in EOC samples. Immunohistochemistry analysis revealed a positive correlation of CD8 and FOXP3 staining with activin A at the protein level in both primary and metastatic epithelial ovarian cancer samples. Furthermore, Activin-A (inhibin-βA) is significantly elevated in EOC patient ascites.

Conclusion: INHBA expression is elevated within EOC, correlating with worse survival, with activin protein levels correlating with specific immune infiltration. Our findings suggest that activin-A may play a role in suppressing anti-tumor immunity in EOC, highlighting its potential as a therapeutic target.

Keywords: activin; metastasis; ovarian cancer; tumor immune infiltration.

MeSH terms

  • Activins* / genetics
  • Activins* / metabolism
  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism
  • Carcinoma, Ovarian Epithelial* / genetics
  • Carcinoma, Ovarian Epithelial* / immunology
  • Carcinoma, Ovarian Epithelial* / metabolism
  • Carcinoma, Ovarian Epithelial* / mortality
  • Carcinoma, Ovarian Epithelial* / pathology
  • Female
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Inhibin-beta Subunits* / genetics
  • Inhibin-beta Subunits* / metabolism
  • Lymphocytes, Tumor-Infiltrating / immunology
  • Lymphocytes, Tumor-Infiltrating / metabolism
  • Middle Aged
  • Ovarian Neoplasms* / genetics
  • Ovarian Neoplasms* / immunology
  • Ovarian Neoplasms* / metabolism
  • Ovarian Neoplasms* / mortality
  • Ovarian Neoplasms* / pathology

Substances

  • Inhibin-beta Subunits
  • inhibin beta A subunit
  • Activins
  • INHBB protein, human
  • activin A
  • Biomarkers, Tumor
  • Forkhead Transcription Factors