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  11. The Stromal Microenvironment Endows Pancreatic Neuroendocrine Tumors With Spatially Specific Invasive And Metastatic Phenotypes.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. The Stromal Microenvironment Endows Pancreatic Neuroendocrine Tumors With Spatially Specific Invasive And Metastatic Phenotypes.

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The stromal microenvironment endows pancreatic neuroendocrine tumors with spatially specific invasive and metastatic phenotypes.

Zeng Ye1, Qiang Li2, Yuheng Hu1

  • 1Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Center for Neuroendocrine Tumors, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Shanghai Pancreatic Cancer Institute, Shanghai, 200032, China; Pancreatic Cancer Institute, Fudan University, Shanghai, 200032, China.

Cancer Letters
|March 4, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Cancer-associated fibroblasts (CAFs) drive tumor growth and metastasis in pancreatic neuroendocrine tumors. Myofibroblastic CAFs promote epithelial-mesenchymal transition (EMT) and liver metastasis through TGF-β signaling.

Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment Research

Background:

  • Cancer-associated fibroblasts (CAFs) are crucial in various cancers, but their role in nonfunctional pancreatic neuroendocrine tumors (NF-PanNETs) is understudied.
  • Tumor stroma heterogeneity can influence malignant phenotypes in NF-PanNETs.

Purpose of the Study:

  • To investigate the role of CAF heterogeneity in NF-PanNETs.
  • To elucidate the mechanisms by which CAFs contribute to tumor growth and metastasis in NF-PanNETs.

Main Methods:

  • Analysis of stromal proportion and growth patterns in NF-PanNET patient samples.
  • Spatial profiling of myofibroblastic CAFs (myCAFs) and their proximity to tumor cells.
  • Investigation of TGF-β signaling pathways involved in epithelial-mesenchymal transition (EMT).
Keywords:
Cell interactionSpatial heterogeneityTumor cell plasticityTumor stroma

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Main Results:

  • High stromal proportion, particularly infiltrating stroma, correlated with poor prognosis in NF-PanNET patients.
  • Myofibroblastic CAFs (FAP+, α-SMAhigh) were spatially associated with tumor cells and promoted EMT and tumor growth.
  • myCAFs induced EMT in adjacent tumor cells via TGF-β signaling, leading to distant metastasis and liver metastasis.

Conclusions:

  • myCAFs contribute to spatial heterogeneity of EMT in NF-PanNETs, driving liver metastasis.
  • Targeting myCAF-mediated TGF-β signaling may offer strategies for preventing liver metastasis in NF-PanNETs.