An EMT-based gene signature enhances the clinical understanding and prognostic prediction of patients with ovarian cancers

J Ovarian Res. 2023 Mar 13;16(1):51. doi: 10.1186/s13048-023-01132-2.

Abstract

Background: Ovarian cancer (OC) is one of the most common gynecological cancers with malignant metastasis and poor prognosis. Current evidence substantiates that epithelial-mesenchymal transition (EMT) is a critical mechanism that drives OC progression. In this study, we aspire to identify pivotal EMT-related genes (EMTG) in OC development, and establish an EMT gene-based model for prognosis prediction.

Methods: We constructed the risk score model by screening EMT genes via univariate/LASSO/step multivariate Cox regressions in the OC cohort from TCGA database. The efficacy of the EMTG model was tested in external GEO cohort, and quantified by the nomogram. Moreover, the immune infiltration and chemotherapy sensitivity were analyzed in different risk score groups.

Results: We established a 11-EMTGs risk score model to predict the prognosis of OC patients. Based on the model, OC patients were split into high- and low- risk score groups, and the high-risk score group had an inevitably poor survival. The predictive power of the model was verified by external OC cohort. The nomogram showed that the model was an independent factor for prognosis prediction. Moreover, immune infiltration analysis revealed the immunosuppressive microenvironment in the high-risk score group. Finally, the EMTG model can be used to predict the sensitivity to chemotherapy drugs.

Conclusions: This study demonstrated that EMTG model was a powerful tool for prognostic prediction of OC patients. Our work not only provide a novel insight into the etiology of OC tumorigenesis, but also can be used in the clinical decisions on OC treatment.

Keywords: Chemotherapy; EMT; Immune infiltration; Ovarian cancer; Prognosis.

MeSH terms

  • Epithelial-Mesenchymal Transition*
  • Female
  • Humans
  • Nomograms
  • Ovarian Neoplasms*
  • Prognosis
  • Risk Factors
  • Tumor Microenvironment