DSG2 promotes pancreatic cancer stem cell maintenance via support of tumour and macrophage cellular cross-talk

Cell Death Dis. 2025 Jul 4;16(1):492. doi: 10.1038/s41419-025-07833-4.

Abstract

Pancreatic cancer stem cells (PCSCs) are a small population of cells in tumours that exhibit enhanced self-renewal and differentiation capabilities. CSCs proactively remodel the tumour microenvironment to maintain CSC stemness, which contributes to chemotherapy resistance. Compared with targeting PCSCs themselves, targeting the PCSC niche may be a novel strategy for pancreatic cancer (PC) therapy. Here, we found that DSG2, a member of the desmosomal cadherin family, is highly expressed in PCSCs. DSG2 upregulation is correlated with adverse outcomes in PC patients. DSG2 knockdown suppressed IL-4 and GM-CSF expression, which promoted the enrichment of tumour-associated macrophages to establish a supportive PCSC niche. Furthermore, we found that the IL-8/CXCR2 axis interacts with DSG2 to promote PCSC stemness and gemcitabine resistance by activating the Wnt/β-catenin pathway. These findings highlight the novel regulatory mechanism of DSG2 in PC, providing new targets for the development of therapeutics targeting PCSC niches.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Deoxycytidine / analogs & derivatives
  • Deoxycytidine / pharmacology
  • Desmoglein 2* / genetics
  • Desmoglein 2* / metabolism
  • Drug Resistance, Neoplasm
  • Gemcitabine
  • Humans
  • Macrophages* / metabolism
  • Macrophages* / pathology
  • Mice
  • Neoplastic Stem Cells* / drug effects
  • Neoplastic Stem Cells* / metabolism
  • Neoplastic Stem Cells* / pathology
  • Pancreatic Neoplasms* / genetics
  • Pancreatic Neoplasms* / metabolism
  • Pancreatic Neoplasms* / pathology
  • Tumor Microenvironment
  • Tumor-Associated Macrophages* / metabolism
  • Wnt Signaling Pathway

Substances

  • Desmoglein 2
  • DSG2 protein, human
  • Deoxycytidine
  • Gemcitabine