Common cold virus could target and disrupt cancer cells
A novel mechanism used by adenovirus to sidestep the cell's suicide program, could go a long way to explain how tumour suppressor genes are silenced in tumour cells and pave the way for a new type of targeted cancer therapy, report researchers at the Salk Institute for Biological Studies in the Aug. 26, 2010 issue of Nature.
When a cell is under stress, the tumour suppressor p53 springs into action activating an army of foot soldiers that initiate a built-in "auto-destruct" mechanism that eliminates virus-infected or otherwise abnormal cells from the body. Just like tumour cells, adenoviruses, which cause upper-respiratory infections, need to get p53 out of the way to multiply successfully.
"Instead of inactivating p53 directly, adenovirus renders the 'guardian of the genome' powerless by targeting the genome itself," explains Dr Clodagh O'Shea, an assistant professor in the Molecular and Cell Biology Laboratory, who led the study. "It literally creates zip files of p53 target genes by compressing them till they can no longer be read."
The p53 tumour suppressor pathway is inactivated in almost every human cancer, allowing cells to escape normal growth controls. Yet there is still no rationally designed targeted cancer therapy to treat patients based on the loss of p53.
Read the whole article at ecancermedicalscience
Reference
- Soria, C., Estermann, F. E., Espantman, K. C., O’Shea, C.C. Heterochromatin silencing of p53 target genes by a small viral protein. Nature, 2010; 466 (7310): 1076 DOI: 10.1038/nature09307
Keywords: p53, adenovirus, tumour suppressor genes, oncolytic cancer therapy
30. 8. 2010 ecancermedicalscience
