Type I interferon (IFN) was originally identified as an immunomodulatory cytokine because of its antiviral activity. Further characterization of its biological effects revealed a prominent role in the direct control of cell growth and potent immunomodulatory and antiangiogenic actions. IFN-α and IFN-ß had both been classified as type I IFN, but differences in their antitumor activities were reported. We confirmed the difference in the antiproliferative activities of IFN-α2b and IFN-ß toward HT29 and SW480 cells. IFN treatment was observed to prolong cell cycle progression; in particular, the accumulation of S-phase population was one of the most characteristic changes. The prolongation of S-phase progression and transition into G2/M-phase was suggested to be a crucial action of type I IFN on colon cancer. Additionally, IFN activated the p21 promoter gene and induced p21 WAF1/CIP1 expression. Furthermore, the cell cycle prolongation effect of IFN was suppressed when p21 expression was downregulated. Therefore, we confirmed that p21 WAF1/CIP1 was a crucial target molecule for the effects of IFN on the cell cycle. Additionally, the ability of p21 induction differed between IFN-α2b and IFN-ß and correlated with their inhibitory activities toward cell growth. We conclude that type I IFN prolongs cell cycle progression by p21 WAF1/CIP1 induction in human colon cancer cells.
The gtjT gene and its upstream region isolated from the Streptococcus sobrinus OMZ176 chromosomal DNA were sequenced. The g(JT gene was preceded by a potential Shine-Dalgarno sequence. The g(fT gene product, glucosyltransferase (GTF), displays a typical gram-positive bacterial signal peptide sequence and both an active site peptide sequence and carboxy-terminal repeats typical of GTFs. The signal sequence is similar to those of other known GTF proteins. The putative active-site peptide sequence of this enzyme was DGIRVDAVD, which was different by one amino acid from the active-site peptide sequence derived from two different types of the S. sobyinus GTFs reported previously (G.
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