Published online Apr 7, 2015. doi: 10.3748/wjg.v21.i13.3876
Peer-review started: August 4, 2014
First decision: August 27, 2014
Revised: September 21, 2014
Accepted: November 30, 2014
Article in press: December 1, 2014
Published online: April 7, 2015
Processing time: 247 Days and 2.1 Hours
AIM: To evaluate/isolate cancer stem cells (CSCs) from tissue or cell lines according to various definitions and cell surface markers.
METHODS: Lectin microarray analysis was conducted on CSC-like fractions of the human pancreatic cancer cell line Panc1 by establishing anti-cancer drug-resistant cells. Changes in glycan structure of CSC-like cells were also investigated in sphere-forming cells as well as in CSC fractions obtained from overexpression of CD24 and CD44.
RESULTS: Several types of fucosylation were increased under these conditions, and the expression of fucosylation regulatory genes such as fucosyltransferases, GDP-fucose synthetic enzymes, and GDP-fucose transporters were dramatically enhanced in CSC-like cells. These changes were significant in gemcitabine-resistant cells and sphere cells of a human pancreatic cancer cell line, Panc1. However, downregulation of cellular fucosylation by knockdown of the GDP-fucose transporter did not alter gemcitabine resistance, indicating that increased cellular fucosylation is a result of CSC-like transformation.
CONCLUSION: Fucosylation might be a biomarker of CSC-like cells in pancreatic cancer.
Core tip: Fucosylation is one of the most important glycosylation events involved in cancer and inflammation. In the present study, we investigated oligosaccharide modifications in pancreatic cancer cancer stem cell (CSC)-like cells. Using several models of CSC-like cells, we found that fucosylation is a common type of glycosylation change in pancreatic cancer CSC-like cells. CSCs are known to be preferentially resistant to many current therapies, including various chemotherapeutic agents and radiation treatment. Our present study suggests that the identification of fucosylated glycoproteins derived from pancreatic cancer cells could lead to novel biomarker development for anticancer drug resistance.