AI Article Synopsis
- Cyclin D1 promotes cell cycle progression in normal cells, but it is also an oncogene that can lead to cancer by allowing cells to bypass normal growth signals.
- Cyclin D1 overexpression in tumors is linked to chromosome abnormalities, although it hasn't been fully proven to cause these issues in lab experiments.
- In this study, cyclin D1 caused significant mitotic abnormalities and cell death in liver and breast cells, suggesting it can disrupt normal cell division and contribute to cancer development.
Article Abstract
In normal cells, cyclin D1 is induced by growth factors and promotes progression through the G(1) phase of the cell cycle. Cyclin D1 is also an oncogene that is thought to act primarily by bypassing the requirement for mitogens during the G(1) phase. Studies of clinical tumors have found that cyclin D1 overexpression is associated with chromosome abnormalities, although a causal effect has not been established in experimental systems. In this study, we found that transient expression of cyclin D1 in normal hepatocytes in vivo triggered dysplastic mitoses, accumulation of supernumerary centrosomes, abnormalities of the mitotic spindle, and marked chromosome changes within several days. This was associated with up-regulation of checkpoint genes p53 and p21 as well as hepatocyte apoptosis in the liver. Transient transfection of cyclin D1 also induced centrosome and mitotic spindle abnormalities in breast epithelial cells, suggesting that this may be a generalized effect. These results indicate that cyclin D1 can induce deregulation of the mitotic apparatus and aneuploidy, effects that could contribute to the role of this oncogene in malignancy.
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| http://dx.doi.org/10.1074/jbc.M407105200 | DOI Listing |
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