IRF-1- mediated CAS expression enhances interferon-gamma-induced apoptosis of HT-29 colon adenocarcinoma cells.
The expression of CAS is reported to be upregulated in a variety of human tumor cells, and such expression correlates with the development of tumors. CAS also plays a role in apoptosis. We investigated whether CAS expression affects the susceptibility of tumor cells to IFN-gamma-induced apoptosis. Our data show that IFN-gamma treatment induces CAS expression in HT-29 tumor cells. IFN-gamma-induced gene expression is primarily mediated by the transcriptional factor, IRF-1. Our data show that IRF-1 mediates IFN-gamma- induced CAS expression. Transfection of HT-29 cells with CAS expression vector did not induce apoptosis of cells; nevertheless, CAS overexpression greatly enhanced IFN-gamma-induced apoptosis of cells. CPP32 is regarded as one of the central apoptosis executioner molecules. CAS overexpression enhances IFN-gamma- induced CPP32 expression. These results indicate that tumor cells highly expressing CAS may be more susceptible to apoptosis induced by reagents that are capable of inducing CAS expression. Thus, CAS may be a target for the elimination of tumors.[1]References
- IRF-1-mediated CAS expression enhances interferon-gamma-induced apoptosis of HT-29 colon adenocarcinoma cells. Jiang, M.C., Lin, T.L., Lee, T.L., Huang, H.T., Lin, C.L., Liao, C.F. Mol. Cell Biol. Res. Commun. (2001) [Pubmed]
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