| First Author | Vail ME | Year | 2002 |
| Journal | Oncogene | Volume | 21 |
| Issue | 10 | Pages | 1548-55 |
| PubMed ID | 11896583 | Mgi Jnum | J:75329 |
| Mgi Id | MGI:2176328 | Doi | 10.1038/sj.onc.1205212 |
| Citation | Vail ME, et al. (2002) Bcl-2 expression delays hepatocyte cell cycle progression during liver regeneration. Oncogene 21(10):1548-55 |
| abstractText | Bcl-2 is the prototype of a family of genes that prevent apoptosis. However, several reports indicate that Bcl-2 may also act as a cell cycle modulator. In several human tumors, Bcl-2 expression correlates with a more favorable prognosis and lower tumor proliferative activity. We have shown that Bcl-2 expression delays liver tumor development in transgenic mice even when the gene is turned on shortly before the time of tumor development. We hypothesized that Bcl-2 may delay liver tumorigenesis by interfering with hepatocyte proliferation. To test whether Bcl-2 expression may act on hepatocyte replication we studied liver regeneration in Bcl-2 transgenic mice and wild-type littermates. DNA replication was delayed by approximately 8 h in Bcl-2 transgenic mice compared to the timing of the response in wild-type littermates. Cyclin D expression showed no alterations in the regenerating liver of Bcl-2 transgenic mice. In contrast, there was a delay in the expression of p107, cyclin E and in the activity of cyclin E/cdk 2 activity. These results show that Bcl-2 expression delays cell cycle progression in hepatocytes and suggests that it acts at a step involving cyclin E and p107. DOI: 10.1038/sj/onc/1205212 |
