Inhibition of GSK-3beta enhances reovirus-induced apoptosis in colon cancer cells

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Title
Inhibition of GSK-3beta enhances reovirus-induced apoptosis in colon cancer cells
Author(s)
H J Min; Sang Seok Koh; I R Cho; R Srisuttee; E H Park; B H Jhun; Y G Kim; S Oh; J E Kwak; R N Johnston; Y H Chung
Bibliographic Citation
International Journal of Oncology, vol. 35, no. 3, pp. 617-624
Publication Year
2009
Abstract
Reovirus functions as an oncolytic agent for many types of cancer including colon cancer. Although most studies have emphasized the role of activated Ras signaling in enhancing reoviral oncolysis in susceptible cells, we note that many colon cancers also display elevated ß-catenin. Thus, it is possible that enhanced ß-catenin may augment reoviral susceptibility in colon cancer cells. To explore this hypothesis, HEK293 cells were treated with the glycogen synthase kinase (GSK)-3ß inhibitor LiCl, thereby inducing ß-catenin, followed by reoviral infection. Co-administration with LiCl indeed enhanced cell death compared to reovirus infection alone, but this was not associated with elevated reoviral replication. Similarly, HEK293 cells expressing the Frizzled-1 receptor in Wnt3a-conditioned medium also showed reovirus replication equivalent to that in cells in control medium, further suggesting that up-regulation of ß-catenin does not enhance the replication of reovirus. Instead, we observed that inhibition of GSK-3ß with LiCl decreased reovirus-induced NF-κB activation, leading to accelerated apoptosis via ?
Keyword
reovirusglycogen synthase kinase-3ßß-cateninnuclear factor-κBcolon cancer
ISSN
1019-6439
Publisher
Spandidos Publ Ltd
DOI
http://dx.doi.org/10.3892/ijo_00000373
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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