ArticleJournal of ovarian research2024
Novel prognostic marker TGFBI affects the migration and invasion function of ovarian cancer cells and activates the integrin αvβ3-PI3K-Akt signaling pathway.
Article in Journal of ovarian research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 14 citations in OpenAlex.
- Tumor-associated macrophages and platelets in tumor microenvironment and its potential therapeutic role in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Smoking-Induced STC2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Anti-metastatic potential of flavonoids for the treatment of cancers: focus on epithelial-mesenchymal transition (EMT) process.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1.Oncology reports · 2025Article
- TGFBI promotes EMT and perineural invasion of pancreatic cancer via PI3K/AKT pathway.Medical oncology (Northwood, London, England) · 2025Article
- Processed Products ofAnti-cancer agents in medicinal chemistry · 2025Article
- Low-dose letrozole-HMG regimen reverses letrozole-induced endometrial impairment and improves frozen embryo transfer outcomes.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
backgroundIndividual patients with ovarian cancer show remarkably different prognosis. Present prognostic models for ovarian cancer mainly focus on clinico-pathological parameters, so quantifiable prognostic markers at molecular level are urgently needed. Platelets contribute to ovarian cancer progression, but have not been considered as biomarkers likely due to their instability. Here, we aimed to search for a stable prognostic marker from platelet-treated ovarian cancer cells, and explore its functions and mechanisms.
methodsMicroarrays analysis was done with platelet-treated SKOV-3 ovarian cancer cells. Relevant studies were searched in the Gene Expression Omnibus (GEO) database. The candidate genes were determined by differentially expressed genes (DEGs), Venn diagram drawing, protein-protein interaction (PPI) network, Cox proportional hazards model and Kaplan-Meier analysis. The expression of TGFBI in clinical samples was assessed by immunehistochemical staining (IHC), and the association of TGFBI levels with the clinic-pathological characteristics and prognosis in ovarian cancer patients was evaluated by univariate and multivariate analysis. The functions of TGFBI were predicted using data from TCGA, and validated by in vitro and in vivo experiments. The mechanism exploration was performed based on proteomic analysis, molecular docking and intervention study.
resultsTGFBI was significantly higher expressed in the platelet-treated ovarian cancer cells. An analysis of bioinformatics data revealed that increased expression of TGFBI led to significant decrease of overall survival (OS), progression-free survival (PFS) and post-progression survival (PPS) in ovarian cancer patients. Tissue microarray results showed that TGFBI was an independent factor for ovarian cancer, and TGFBI expression predict poor prognosis. Functionally, TGFBI affected the migration and invasion of ovarian cancer cells by regulation of epithelial mesenchymal transition (EMT) markers (CDH1 and CDH2) and extracellular matrix (ECM) degradation proteins (MMP-2). Mechanistically, TGFBI phosphorylated PI3K and Akt by combining integrin αvβ3.
conclusionsWe found out TGFBI as a novel prognostic indicator for ovarian cancer patients. TGFBI could promote metastasis in ovarian cancer by EMT induction and ECM remodeling, which might be associated with the activation of integrin αvβ3-PI3K-Akt signaling pathway.
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