Systemic Depletion of Nerve Growth Factor Inhibits Disease Progression in a Genetically Engineered Model of Pancreatic Ductal Adenocarcinoma

Pancreas. 2018 Aug;47(7):856-863. doi: 10.1097/MPA.0000000000001090.

Abstract

Objectives: In patients with pancreatic ductal adenocarcinoma (PDAC), increased expression of proinflammatory neurotrophic growth factors (eg, nerve growth factor [NGF]) correlates with a poorer prognosis, perineural invasion, and, with regard to NGF, pain severity. We hypothesized that NGF sequestration would reduce inflammation and disease in the KPC mouse model of PDAC.

Methods: Following biweekly injections of NGF antibody or control immunoglobulin G, beginning at 4 or 8 weeks of age, inflammation and disease stage were assessed using histological, protein expression, and quantitative polymerase chain reaction analyses.

Results: In the 8-week anti-NGF group, indicators of neurogenic inflammation in the dorsal root ganglia (substance P and calcitonin gene-related peptide) and spinal cord (glial fibrillary acidic protein) were significantly reduced. In the 4-week anti-NGF group, TRPA1 mRNA in dorsal root ganglia and spinal phosphorylated ERK protein were elevated, but glial fibrillary acidic protein expression was unaffected. In the 8-week anti-NGF group, there was a 40% reduction in the proportion of mice with microscopic perineural invasion, and no macrometastases were observed.

Conclusions: Anti-NGF treatment beginning at 4 weeks may increase inflammation and negatively impact disease. Treatment starting at 8 weeks (after disease onset), however, reduces neural inflammation, neural invasion, and metastasis. These data indicate that NGF impacts PDAC progression and metastasis in a temporally dependent manner.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / pharmacology*
  • Carcinoma, Pancreatic Ductal / genetics
  • Carcinoma, Pancreatic Ductal / metabolism
  • Carcinoma, Pancreatic Ductal / prevention & control*
  • Disease Models, Animal*
  • Disease Progression
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Ganglia, Spinal / drug effects
  • Ganglia, Spinal / metabolism
  • Gene Expression / drug effects
  • Humans
  • Mice, Transgenic
  • Nerve Growth Factor / antagonists & inhibitors*
  • Nerve Growth Factor / immunology
  • Nerve Growth Factor / metabolism
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / prevention & control*
  • Phosphorylation / drug effects
  • Receptor, trkA / genetics
  • Receptor, trkA / metabolism
  • TRPA1 Cation Channel / genetics
  • TRPA1 Cation Channel / metabolism

Substances

  • Antibodies
  • TRPA1 Cation Channel
  • Trpa1 protein, mouse
  • Nerve Growth Factor
  • Receptor, trkA
  • Extracellular Signal-Regulated MAP Kinases