Cancer cells have been described as immortal because, unlike normal cells, they don’t age and die, but instead can continue to multiply without end.
In most cases, cancer cells become immortal by invoking a genetic mutation that can trigger the production of an enzyme, known as telomerase, which prevents telomeres from shortening. Telomeres are important because they prevent DNA-containing chromosomes from damage or fusing with nearby chromosomes. The longer the telomere, the better protected the chromosome and the DNA within it.
But there is another, less understood way how cancer cells achieve immortality. In a new study, University of Iowa biologist Anna Malkova explored Alternative Lengthening of Telomeres (ALT), a second pathway that cancer cells employ to maintain telomeres. Malkova and Josep Comeron, professor of biology at Iowa, analyzed baker’s yeast to solve two issues: the frequency of ALT and the structure of ALT chromosome ends.
“We overcame these problems and determined the frequency of ALT and the structure of ALT survivors in wild type cells, as well as in various ALT-defective mutants,” says Malkova, a professor in the Department of Biology. “This allowed us to demonstrate that, contrary to the current view, both RAD51-dependent and independent mechanisms are required for a one unified ALT survivor pathway.”
The researchers say a similar, unified ALT pathway may operate in other organisms including humans.
The study was published online in the journal Molecular Cell.
Source: University of Iowa