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An integrated study to decipher immunosuppressive cellular communication in the PDAC environment.

Gülben Avşar1,2, Pınar Pir3

  • 1Department of Bioengineering, Gebze Technical University, Kocaeli, Turkey. g.avsar@gtu.edu.tr.

NPJ Systems Biology and Applications
|November 9, 2023
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Tumor-associated macrophages (TAMs) drive an immunosuppressive tumor microenvironment in pancreatic cancer. Targeting the LGALS9 gene, upregulated in TAMs, may offer new pancreatic ductal adenocarcinoma immunotherapy strategies.

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Area of Science:

  • Oncology
  • Immunology
  • Genomics

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with a rigid, immunosuppressive tumor microenvironment (TME).
  • Cellular interactions within the TME are critical for immune evasion, chemoresistance, and poor prognosis in PDAC.
  • Understanding cellular crosstalk is essential for developing effective PDAC treatments.

Purpose of the Study:

  • To decipher cellular communication within the PDAC TME.
  • To identify key cell types and molecular players regulating the PDAC microenvironment.
  • To explore potential therapeutic targets for PDAC immunotherapy.

Main Methods:

  • Integration of spatial transcriptomics, single-cell RNA sequencing (scRNA-seq), and bulk RNA-seq datasets.
  • Analysis of cellular interactions and gene expression profiles in PDAC samples.
  • Comparative analysis of gene expression in tumor-associated macrophages (TAMs) versus tumor-suppressor immune cells.

Main Results:

  • Tumor-associated macrophages (TAMs) are central regulators of the PDAC TME, promoting immunosuppression.
  • LGALS9 gene expression is upregulated in PDAC tumors and specifically in TAMs compared to other immune cells.
  • LGALS9 is a primary mediator of crosstalk between TAMs and other cells, with P4HB showing notable interaction.

Conclusions:

  • TAMs play a significant role in PDAC progression through the LGALS9 gene.
  • The interaction between LGALS9 and P4HB presents a potential therapeutic target for PDAC.
  • Targeting TAM-mediated immunosuppression via LGALS9 could enhance combinatory immunotherapies for pancreatic cancer.