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Defensin-Rich Platelets Drive Pro-Tumorigenic Programs in Pancreatic Adenocarcinoma.

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Platelets contain alpha-defensins (DEFA1/3) that promote pancreatic cancer (PDAC) growth and spread. Targeting these platelet molecules may offer new therapeutic strategies for aggressive PDAC.

Keywords:
DEFA1/3alpha-defensinspancreatic cancerparticles like-plateletsplateletstranscriptomicstumor progressionzebrafish xenograft

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Area of Science:

  • Oncology
  • Hematology
  • Molecular Biology

Background:

  • Pancreatic Ductal Adenocarcinoma (PDAC) is a lethal cancer with limited treatment options.
  • Platelets, beyond hemostasis, actively influence tumor progression and serve as potential biomarkers.
  • The role of platelet alpha-defensins (DEFA1/3) in PDAC pathogenesis is largely unknown.

Purpose of the Study:

  • To investigate the impact of DEFA1/3 in PDAC progression.
  • To explore the functional role of DEFA1/3 in platelet-tumor cell interactions.
  • To identify DEFA1/3 as a potential biomarker and therapeutic target in PDAC.

Main Methods:

  • Bioinformatic analysis of platelet transcriptomes.
  • In vitro functional assays using pancreatic cancer cells.
  • In vivo zebrafish xenograft models to assess tumor dissemination.
  • Analysis of The Cancer Genome Atlas (TCGA)-PDAC clinical data.

Main Results:

  • DEFA1/3 expression was significantly upregulated in PDAC-derived platelets.
  • Defensin-enriched platelet-like particles (DRPs) and recombinant DEFA1/3 increased cancer cell proliferation, migration, and 3D growth in vitro.
  • DEFA1/3 promoted tumor dissemination in zebrafish xenografts.
  • High DEFA1/3 expression correlated with poor survival, increased immune infiltration, and EMT activation in PDAC patients.

Conclusions:

  • Platelet-derived DEFA1/3 functionally modulates PDAC progression.
  • DEFA1/3 links platelet granule content to tumor aggressiveness.
  • DEFA1/3 represents a potential biomarker and therapeutic target in the platelet-tumor axis for PDAC.