The role of S100A9 in the interaction between pancreatic ductal adenocarcinoma cells and stromal cells

Cancer Immunol Immunother. 2022 Mar;71(3):705-718. doi: 10.1007/s00262-021-03026-y. Epub 2021 Aug 10.

Abstract

Background: A major feature of the microenvironment in pancreatic ductal adenocarcinoma (PDAC) is the significant amount of extracellular matrix produced by pancreatic stellate cells (PSCs), which have been reported to enhance the invasiveness of pancreatic cancer cells and negatively impact the prognosis.

Methods: We analyzed the data from two publicly available microarray datasets deposited in the Gene Expression Omnibus and found candidate genes that were differentially expressed in PDAC cells with metastatic potential and PDAC cells cocultured with PSCs. We studied the interaction between PDAC cells and PSCs in vitro and verified our finding with the survival data of patients with PDAC from the website of The Human Protein Atlas.

Results: We found that PSCs stimulated PDAC cells to secrete S100A9, which attracted circulatory monocytes into cancer tissue and enhanced the expression of programmed death-ligand 1 (PD-L1) on macrophages. When analyzing the correlation of S100A9 and PD-L1 expression with the clinical outcomes of patients with PDAC, we ascertained that high expression of S100A9 and PD-L1 was associated with poor survival in patients with PDAC.

Conclusions: PSCs stimulated PDAC cells to secrete S100A9, which acts as a chemoattractant to attract circulatory monocytes into cancer microenvironment and induces expression of PD-L1 on macrophages. High expression of S100A9 and PD-L1 was associated with worse overall survival in a cohort of patients with PDAC.

Keywords: PD-L1; PSC; Pancreatic ductal adenocarcinoma; S100A9.

MeSH terms

  • Biomarkers
  • Calgranulin B / genetics*
  • Calgranulin B / metabolism
  • Cancer-Associated Fibroblasts / metabolism
  • Cancer-Associated Fibroblasts / pathology
  • Carcinoma, Pancreatic Ductal / etiology*
  • Carcinoma, Pancreatic Ductal / metabolism*
  • Carcinoma, Pancreatic Ductal / mortality
  • Carcinoma, Pancreatic Ductal / pathology
  • Cell Communication* / genetics
  • Cell Communication* / immunology
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Coculture Techniques
  • Culture Media, Conditioned / pharmacology
  • Disease Susceptibility
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Humans
  • Neoplasm Grading
  • Neoplasm Staging
  • Pancreatic Neoplasms / etiology*
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / mortality
  • Pancreatic Neoplasms / pathology
  • Pancreatic Stellate Cells / metabolism
  • Pancreatic Stellate Cells / pathology
  • Prognosis
  • RNA Interference
  • Stromal Cells / metabolism*
  • Stromal Cells / pathology
  • Tumor Microenvironment / genetics
  • Tumor Microenvironment / immunology

Substances

  • Biomarkers
  • Calgranulin B
  • Culture Media, Conditioned
  • S100A9 protein, human