An enzyme that can make cells live forever has been touted as a key to understanding aging and treating diseases from AIDS to diabetes. However, the enzyme may also turn on a gene that stimulates cancer, researchers report in the 15 June issue of Nature. Other researchers worry that the finding may be due to laboratory artifacts.
Telomerase immortalizes cells by protecting the tips of their chromosomes, which are known as telomeres. Telomeres dictate how many times a cell can divide: With each division, a bit of these chromosome caps chips away. When the caps are gone, the cell can no longer replicate. Telomerase rebuilds the telomeres and allows cells to divide--potentially forever. So scientists hope to use the enzyme to grow unlimited amounts of human cells in culture, including skin cells for burn victims, insulin-secreting cells for diabetics, and new white blood cells for AIDS patients. But some researchers fear that telomerase could make cells divide uncontrollably. Indeed, the enzyme is present in nearly all cancer cells, but isn't found in most normal mature cells, which suggests that telomerase might trigger unfettered cell multiplication.
To investigate this possibility, molecular biologist David Beach of University College, London, and two colleagues in the United States grew human breast epithelial cells in a culture. Then they infected them with a virus carrying the telomerase gene. As expected, the cells incorporated the gene and were still going strong after 250 divisions, about four times their normal life span. But during cell growth the activity of another gene called c-myc jumped two to three times higher than normal. This gene is cranked up in several kinds of cancers, including breast cancer and some lymphomas, so although the cultured cells probably weren't cancerous, Beach says, they had taken an ominous step in that direction.
The results show that researchers must know more about how cells age before they can safely use telomerase to grow replacement tissue, Beach says. But cell biologist Jerry Shay of the University of Texas Southwestern Medical Center in Dallas thinks that the cancer gene may have been turned on simply because of the way the cells were grown in the laboratory. Shay says this could be a case of "much ado about tissue culture artifacts."