PAUF promotes adhesiveness of pancreatic cancer cells by modulating focal adhesion kinase.
10.3858/emm.2011.43.5.030
- Author:
Yangsoon LEE
1
;
Su Jin KIM
;
Hye Jin MIN
;
Ji Yoon JO
;
Eun Hye PARK
;
Sang Seok KOH
Author Information
1. Therapeutic Antibody Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea. sskoh@kribb.re.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
adhesion;
anoikis;
FAK;
PAUF;
pancreatic cancer;
signaling
- MeSH:
Anoikis/genetics;
Cell Line, Tumor;
Focal Adhesion Protein-Tyrosine Kinases/*metabolism;
Focal Adhesions/genetics/*metabolism;
Humans;
Lectins/genetics/*metabolism;
Pancreatic Neoplasms/enzymology/genetics/*metabolism;
Proto-Oncogene Proteins pp60(c-src)/metabolism;
Signal Transduction/genetics
- From:Experimental & Molecular Medicine
2011;43(5):291-297
- CountryRepublic of Korea
- Language:English
-
Abstract:
Pancreatic cancer is a notorious disease with a poor prognosis and low survival rates, which is due to limited advances in understanding of the molecular mechanism and inadequate development of effective treatment options over the decades. In previous studies, we demonstrated that a novel soluble protein named pancreatic adenocarcinoma up-regulated factor (PAUF) acts on tumor and immune cells and plays an important role in metastasis and progression of pancreatic cancer. Here we show that PAUF promotes adhesiveness of pancreatic cancer cells to various extracellular matrix (ECM). Our results further support a positive correlation of activation and expression of focal adhesion kinase (FAK), a key player in tumor cell metastasis and survival, with PAUF expression. PAUF-mediated adhesiveness was significantly attenuated upon blockade of the FAK pathway. Moreover, PAUF appeared to enhance resistance of pancreatic cancer cells to anoikis via modulation of FAK. Our results suggest that PAUF-mediated FAK activation plays an important role in pancreatic cancer progression.
