At the cellular level, aging and cancer are two sides of the same coin. The mechanism that limits a cell's lifespan can be slowed down, but that can turn them cancerous, as they divide unchecked. Now, scientists at EPFL have found a way to manipulate that mechanism to effectively turn off cancer's immortality, letting it die slowly and naturally.

Every time a cell divides, it consults the blueprints contained in the chromosomes, but some genetic information is lost with every division. To protect the important bits, the tips of the chromosomes are covered with repeating sequences of "junk" DNA known as telomeres. Eventually even they erode away, leaving the cell vulnerable to damage – which we recognize as wrinkles, grey hairs, decreased metabolism, and higher chances of disease. In that way, telomere length is inextricably linked to aging.

But we have a protector fighting on our side. Telomerase is an enzyme that actively works to counter the natural degradation of telomeres, replenishing them as cells divide. Unfortunately the little crusader's efforts are ultimately in vain, and aging always wins out. Still, that makes this hard-working enzyme a key target in anti-aging research, and scientists are developing ways to boost its levels or supercharge its function.

But telomerase has a dark side. Cancer hijacks it to make tumors virtually immortal. Blocking the enzyme has been tested as one way to fight cancer, but so far it's proved tricky to do.

The new EPFL study has found that rather than tackling telomerase directly, tumors can be made mortal again by targeting their telomeres instead. The researchers discovered two antioxidant enzymes, known as PRDX1 and MTH1, which help protect telomeres from oxidation damage.

The team found that blocking these two enzymes instead had a better result, leaving tumor telomeres vulnerable to damage once again. Although telomerase kept trying to replenish them, it wasn't enough, and the cells eventually died naturally.

"Instead of inhibiting the enzyme itself, we target its substrate – the chromosome end – making it un-extendable by telomerase," says Joachim Lingner, co-author of the study.

The research was published in the journal Genes & Development.

Source: EPFL