RIPK4 Is an Immune Regulating-Associated Biomarker for Ovarian Cancer and Possesses Generalization Value in

Cui Liao1, Yi-Xia Zhao1, Wei-di Han2

  • 1Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Shapingba District, Chongqing 400030, China.

Insights

Receptor interacting serine/threonine kinase 4 (RIPK4) is elevated in ovarian cancer (OC) and linked to poorer survival. This study identifies RIPK4 as a potential prognostic marker for OC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer (OC) is a leading cause of gynecologic cancer mortality.
  • Receptor interacting serine/threonine kinase 4 (RIPK4) expression is altered in various cancers, but its role in OC is understudied.

Purpose of the Study:

  • To investigate the expression, prognostic value, and potential functions of RIPK4 in ovarian cancer.
  • To evaluate RIPK4 as a biomarker for OC patient outcomes.

Main Methods:

  • Analysis of RIPK4 expression in OC and normal tissues using TCGA and GEO datasets.
  • Prognostic value assessment via Kaplan-Meier and multivariate analyses.
  • Functional enrichment analysis (GO, KEGG) and immune cell infiltration estimation (CIBERSORT).
  • Pan-cancer validation of RIPK4's association with survival.

Main Results:

  • RIPK4 expression is significantly higher in OC tissues compared to non-tumor tissues.
  • High RIPK4 expression correlates with shorter overall survival in OC patients.
  • RIPK4 is an independent prognostic factor for OC.
  • Enriched pathways in high RIPK4 tumors include focal adhesion and cancer-related metabolism.
  • RIPK4 expression is positively correlated with tumor-infiltrating immune cells (TICs).

Conclusions:

  • RIPK4 serves as a potential prognostic biomarker for ovarian cancer.
  • RIPK4 dysregulation may influence OC progression and immune microenvironment.
  • Further research into RIPK4's functional mechanisms in OC is warranted.