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World J Gastroenterol. Oct 21, 2013; 19(39): 6555-6558
Published online Oct 21, 2013. doi: 10.3748/wjg.v19.i39.6555
Pleiotrophin promotes perineural invasion in pancreatic cancer
Jun Yao, Xiu-Feng Hu, Xiao-Shan Feng, She-Gan Gao
Jun Yao, Xiu-Feng Hu, Xiao-Shan Feng, She-Gan Gao, Department of Oncology, the First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471003, Henan Province, China
Author contributions: Yao J and Feng XS conceived and designed the study, did literature search and wrote the manuscript; Yao J and Hu XF were involved in the manuscript writing; Gao SG designed the study and wrote the manuscript; all authors have read and approved the final version to be published.
Supported by National Natural Science Foundation of China, No. U1204819; and Health Science and Technology Innovation Talents Program of Henan Province, China, No. 4203
Correspondence to: Xiao-Shan Feng, PhD, MD, Professor, Department of Oncology, the First Affiliated Hospital of Henan University of Science and Technology, 24 Jinghua Road, Luoyang 471003, Henan Province, China. hospitalluo@163.com
Telephone: +86-379-64815783 Fax: +86-379-64815783
Received: June 14, 2013
Revised: July 19, 2013
Accepted: August 5, 2013
Published online: October 21, 2013
Processing time: 147 Days and 0.2 Hours
Abstract

Perineural invasion (PNI) in pancreatic cancer is an important cause of local recurrence, but little is known about its mechanism. Pleiotrophin (PTN) is an important neurotrophic factor. It is of interest that our recent experimental data showed its involvement in PNI of pancreatic cancer. PTN strongly presents in the cytoplasm of pancreatic cancer cells, and high expression of PTN and its receptor may contribute to the high PNI of pancreatic cancer. Correspondingly, PNI is prone to happen in PTN-positive tumors. We thus hypothesize that, as a neurite growth-promoting factor, PTN may promote PNI in pancreatic cancer. PTN is released at the time of tumor cell necrosis, and binds with its high-affinity receptor, N-syndecan on pancreatic nerves, to promote neural growth in pancreatic cancer. Furthermore, neural destruction leads to a distorted neural homeostasis. Neurons and Schwann cells produce more N-syndecan in an effort to repair the pancreatic nerves. However, the abundance of N-syndecan attracts further PTN-positive cancer cells to the site of injury, creating a vicious cycle. Ultimately, increased PTN and N-syndecan levels, due to the continuous nerve injury, may promote cancer invasion and propagation along the neural structures. Therefore, it is meaningful to discuss the relationship between PTN/N-syndecan signaling and PNI in pancreatic cancer, which may lead to a better understanding of the mechanism of PNI in pancreatic cancer.

Keywords: Pleiotrophin; N-syndecan; Neurite outgrowth; Perineural invasion; Pancreatic cancer

Core tip: We discussed the important novel role of pleiotrophin (PTN) in perineural invasion (PNI) of pancreatic cancer, an important cause of local recurrence. Our recent experimental data demonstrated the involvement of PTN in PNI of pancreatic cancer. PTN strongly presents in the cytoplasm of pancreatic cancer cells, and high expression of PTN and its receptor may contribute to the high PNI of pancreatic cancer.