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Updated: Jan 2, 2026

In Vitro Modeling of Cancerous Neural Invasion: The Dorsal Root Ganglion Model
Published on: April 12, 2016
Sonic hedgehog signaling pathway promotes pancreatic cancer pain via nerve growth factor
Liang Han1, Jie Jiang2, Mengwen Xue3
1Department of Hepatobiliary Surgery, Xi'an Jiaotong University Medical College First Affiliated Hospital, Xi'an, Shaanxi, China.
Background:
Many patients with pancreatic cancer (PC) suffer from abdominal pain and back pain. However, the cause of pain associated with PC is largely unclear. In this study, we tested the potential influence of the sonic hedgehog (sHH) signaling pathway on PC pain.
Methods:
Substance P (SP) and calcitonin gene-related peptide (CGRP) expression was measured in cultured PC cells and dorsal root ganglions (DRG) by real-time PCR, western blotting analysis and ELISA. Small interfering RNA transfection and plasmid constructs were used to regulate the expression of sHH in the AsPc-1 and Panc-1 cell lines. Pain-related behavior was observed in an orthotopic tumor model in nude mice.
Results:
In this study, the results show that sHH increased the expression of SP and CGRP in DRGs in a concentration and time-dependent manner. Additionally, sHH secretion from PC cells could activate the sHH signaling pathway and, in turn, increase the expression of nerve growth factor (NGF), P75, and TrkA in DRGs. Furthermore, the sHH signaling pathway and NGF/NGF receptor contributed to pain sensitivity in a nude mouse model.
Conclusion:
Our results demonstrate that PC pain originates from the sHH signaling pathway, and NGF mediates the pain mechanism via regulating SP and CGRP.
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