ArticleDiscover oncology2025
PTTG1 promotes M2 macrophage polarization via the cGMP-PKG signaling pathway and facilitates EMT progression in human epithelial ovarian cancer cells.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Multi-omics reveals soybean meal-induced gut microbiota alterations and metabolic disturbances in largemouth bass (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Comprehensive analysis of metabolic reprogramming-related gene signatures for predicting ovarian cancer prognosis, the immune landscape, and potential treatment options.Discover oncology · 2026Article
- Integrative analysis reveals PRKCB and SRD5A2 as potential immune-associated biomarkers in prostate cancer targeted by traditional Chinese medicine.Frontiers in oncology · 2026Article
- Prognostic value and molecular mechanism of photodynamic therapy and apoptosis related gene FGFR1 in bladder cancer.Frontiers in oncology · 2025Article
- Macrophages and neutrophils in ovarian cancer microenvironment.Frontiers in immunology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Epithelial Ovarian Cancer (EOC) is complex and heterogeneous, making accurate prognosis and treatment prediction difficult. New therapeutic targets and their mechanisms are urgently needed. This study explored the role of PTTG1 in ovarian cancer via the cGMP-PKG signaling pathway, focusing on its effects on M2 macrophage polarization and EMT progression in EOC cells. Using the GSE135886 database, we performed differential gene expression, pathway enrichment, and immune infiltration analyses to identify key targets influencing EMT and macrophage polarization. We then constructed PTTG1 knockdown and overexpression cell lines to assess the impact of PTTG1 on cell proliferation, migration, invasion, EMT, and macrophage polarization in vitro. Analysis revealed that differentially expressed genes were enriched in the cGMP-PKG pathway and correlated with M2 macrophages. PTTG1 overexpression in A2780 and SK-OV-3 ovarian cancer cells promoted proliferation, invasion, and migration, while enhancing sGC, PKG1, and PKG2 expression to activate the cGMP-PKG pathway and induce M2 macrophage polarization. PTTG1 knockdown produced opposite results, reinforcing our conclusions. This study uncovers a novel mechanism of PTTG1 in ovarian cancer development and suggests it as a potential therapeutic target.
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