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Updated: Jan 11, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
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Network Controllability Reveals Key Mitigation Points for Tumor-Promoting Signaling in Tumor-Educated Platelets.

Özge Osmanoglu1, Elif Özer1, Shishir K Gupta1,2

  • 1Functional Genomics & Systems Biology Group, Department of Bioinformatics, Biocenter, Am Hubland, University of Wuerzburg, 97074 Würzburg, Germany.

International Journal of Molecular Sciences
|November 13, 2025
PubMed
Summary
This summary is machine-generated.

Targeting tumor-educated platelets (TEPs) with FDA-approved drugs like fostamatinib may reduce metastasis in non-small-cell lung cancer (NSCLC). This study identified key genes and drug combinations for TEP-specific therapies.

Keywords:
ITAMP2Y12cancernon-small cell lung cancer (NSCLC)signalingtumor-educated platelets (TEP)

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Area of Science:

  • Oncology
  • Hematology
  • Bioinformatics
  • Systems Biology

Background:

  • Tumor-educated platelets (TEPs) play a crucial role in promoting cancer metastasis through complex signaling pathways.
  • Existing therapeutic strategies often overlook the specific contributions of TEPs and their interactions with cancer cells.
  • Identifying key molecular players and actionable targets within TEPs is essential for developing effective anti-cancer treatments.

Purpose of the Study:

  • To perform a comprehensive transcriptome and network analysis of TEPs in non-small-cell lung cancer (NSCLC).
  • To identify critical genes and signaling pathways within TEPs that drive cancer progression.
  • To explore FDA-approved drugs and drug combinations for targeting TEPs and reducing metastasis.

Main Methods:

  • Transcriptome analysis of TEP gene expression data (GSE89843) from NSCLC patients.
  • Integration with protein-protein interaction data to construct a TEP-specific signaling network.
  • Network topology and controllability analysis to identify key nodes and pharmacologically controllable subnetworks.
  • Identification of high-confidence target genes and exploration of FDA-approved drugs.

Main Results:

  • Identified 111 upregulated and 108 downregulated genes in TEPs, enriched in pathways related to extracellular matrix, cytoskeleton, immune signaling, and platelet activation.
  • Highlighted unique TEP profiles in NSCLC, with downregulated ribosomal function, apoptosis, and immune signaling.
  • Identified five high-confidence central genes (ITGA2B, FLNA, GRB2, FCGR2A, APP) and potential drug targets.
  • Fostamatinib (SYK inhibitor) emerged as a top candidate to disrupt ITAM-mediated platelet activation; metalloprotease and cytoskeletal targets were also noted.

Conclusions:

  • Integrative analysis reveals key transcriptional and network alterations in TEPs that are detrimental to NSCLC patients.
  • FDA-approved drugs, including fostamatinib, Aducanumab, and aspirin, show potential for therapeutic targeting of metastasis-promoting TEPs.
  • A preclinical in silico approach identified a promising combination therapy to simultaneously target TEPs and NSCLC, potentially reducing metastasis.