Xenoantigen, an αGal epitope-expression construct driven by the hTERT-promoter, specifically kills human pancreatic cancer cell line View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-10-03

AUTHORS

Tokihiko Sawada, Osamu Yamada, Naoko Yoshimura, Keiko Hatori, Shohei Fuchinoue, Satoshi Teraoka

ABSTRACT

BackgroundWe previously reported the usefulness of the αGal epitope as a target molecule for gene therapy against cancer. To induce cancer cell specific transcription of the αGal epitope, an expression vector which synthesizes the αGal epitope under the control of a promoter region of the human telomerase reverse transcriptase (hTERT), NK7, was constructed.MethodsNK7 was transfected into a human pancreatic carcinoma cell line, MIA cells, and telomerase-negative SUSM-1 cells served controls. Expression of the αGal epitope was confirmed by flow cytometry using IB4 lectin. The susceptibility of transfected MIA cells to human natural antibodies, was examined using a complement-dependent cytotoxic cross-match test (CDC) and a flow cytometry using annexin V.ResultsThe αGal epitope expression was detected only on the cell surfaces of NK7-transfected MIA cells, i.e., not on naive MIA cells or telomerase negative SUSM-1 cells. The CDC results indicated that MIA cells transfected with NK7 are susceptible to human natural antibody-mediated cell killing, and the differences, as compared to NK-7 transfected telomerase negative SUSM-1 cells or telomerase positive naïve MIA cells, were statistically significant. The flow cytometry using annexin V showed a higher number of the apoptotic cells in NK-7 transfected MIA cells than in naïve MIA cells.ConclusionsThe results suggest that αGal epitope-expression, under the control of the hTERT-promoter, may be useful in cancer specific gene therapy. More... »

PAGES

14

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1475-2867-2-14

DOI

http://dx.doi.org/10.1186/1475-2867-2-14

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1032705347

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12392598


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