Relationship between αGal epitope expression and decrease of tumorigenicity in pancreatic adenocarcinoma model
✍ Scribed by Muriel Aubert; Christian Crotte; Liliane Benkoel; Laurence Panicot-Dubois; Jean-Paul Bernard; Dominique Lombardo; Marie-Odile Sadoulet; Eric Mas
- Book ID
- 102501747
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 356 KB
- Volume
- 42
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.20082
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✦ Synopsis
Abstract
The αGal epitope is a carbohydrate structure, Galα1,3Galβ1,4GlcNAc‐R, synthesized on glycoconjugates in many mammals by α1,3galactosyltransferase. Humans do not express this epitope and present in serum large amounts of naturally occuring antibodies, which recognize the αGal epitopes and participate in the hyperacute rejection of xenograft. Studies indicated that the fundamental mechanism of hyperacute rejection involving the αGal epitope expression can be used in cancer therapy. We have previously suggested that the αGal epitope expression by human pancreatic tumoral cells could decrease the tumorigenic behavior of these cells. To determine whether the expression of the αGal epitope can modify the tumorigenicity of pancreatic cancer cells, we used a Syrian golden hamster pancreatic adenocarcinoma experimental model. The expression of αGal epitopes in the Syrian golden hamster pancreatic cancer cell line HaP‐T1 was obtained by selecting stable cell clones transfected with murine α1,3galactosyltransferase gene. The αGal epitope expression resulted in a delay in the tumoral development of HaP‐T1 cells in vivo after allograft transplantation of Syrian golden hamsters (2.5‐fold, P < 0.05) and of nude mice. This result is associated with an 100% increase in survival time of nude mice bearing tumors expressing the αGal epitope. Our results confirm that the cell surface expression of αGal epitope decreases the tumorigenic behavior of pancreatic cancer cells. This novel property may be useful for the development of cancer gene immunotherapy strategy. © 2005 Wiley‐Liss, Inc.