Expression and function of proBDNF in pancreatic cancer

Abstract

Pancreatic cancer is a common gastrointestinal malignancy, which incidence is almost equivalent to its mortality and the average five‐year survival rate is still less than 5%. There is no specific diagnostic marker or complete cure program for pancreatic cancer so far. Both proBDNF and BDNF are widespread in central nervous system, proBDNF may be cleaved to produce BDNF by several different mechanisms. Several studies confirmed that BDNF also expressed in non‐nervous system malignancies such as pancreatic cancer, but there is no literature suggests that proBDNF also present in pancreatic cancer as well. In terms of biological activity, proBDNF may have the opposite effect with BDNF. BDNF may bind to the receptor Trk B and P75NTR, and play an important role in promoting tumor cell proliferation and differentiation, invasion and metastasis, angiogenesis, tolerating chemotherapy and inhibiting tumor cell apoptosis. ProBDNF also can bind P75NTR and Trk B receptors, but it is unclear whether proBDNF play a role in the pathogenesis, invasion and metastasis of pancreatic cancer. By immunohistochemical study, our project group found that compared with normal pancreas, BDNF, proBDNF, P75NTR and Trk B was significantly higher in cell cytoplasm and membrane of human pancreatic carcinoma, which means proBDNF and its receptors also play a role in the pathogenesis of pancreatic cancer. We will further study the possible regulation mechanisms and signal transduction pathways of proBDNF in pancreatic cancer, and investigate deeply the pathogenesis of pancreatic cancer.