Interferon alpha-2b and XXXX combined treatment affects proliferation and gene expression of @entity1 @entity2622 cells.

@entity1 @entity9688 @entity2622 @entity3027 @entity1544 @entity1968
The in vivo and in vitro antitumor effectiveness of IFNs is well documented. Their combination with differentiating agents, such as @entity1968 , has been demonstrated to be a promising therapy for @entity1 with advanced @entity1544 and the cervix. However, the mechanisms that mediate these antitumor responses are not yet known. We studied the epidermoid cell line ME 180 derived from @entity1 @entity2622 to test its responsiveness to @entity3027 -alpha-2b (INTRON A) and @entity1968 (RA). Both agents have demonstrated ability to inhibit the growth of @entity1 cells in a dose- and time-dependent manner. The antiproliferative effect was further increased by the treatment with @entity3027 -alpha-2b and RA combined. In accordance with this result, we found that the combination of the two agents has the effect of increasing the expression of the 2-5A synthetase gene, which is thought to play a key role in antigrowth responses to IFNs. At increased levels of 2-5A synthetase mRNA corresponds a significant increase in 2-5A synthetase activity. Although RA per se has no effect on the 2-5A synthetase expression, when it is combined with @entity3027 -alpha-2b it appears to be able to potentiate the @entity3027 -induced 2-5A synthetase expression. Moreover, the combination of @entity3027 -alpha-2b and RA produces a similar effect also on the expression of the HLA-A2 gene, which has been shown to be induced in @entity1 cells both by @entity3027 -alpha-2b and RA alone. In view of the possible mechanisms of action of the two agents, it is interesting to note that their combination increases, although transiently, the expression of @entity9688 , which codes for a transcription factor that regulates @entity3027 gene expression and is thought to be involved in the regulation of @entity3027 -induced effects and in mediating cell death or apoptosis.
