Blocking Specific Enzymes Could Facilitate Cancer Wipe Out
Telomerase counteracts telomere shortening and cellular senescence in germ cells, stem cells, and cancer cells with the addition of repetitive DNA sequences into the ends of chromosomes.
Telomeres are prone to damage by reactive oxygen species (ROS), but the outcome of oxidation of telomeres on telomere length as well as the mechanisms which shield from ROS-mediated telomere damage aren’t well known.
Now, Joachim Lingner and Wareed Ahmed at the EPFL have discovered two antioxidant enzymes- PRDX1 and MTH1- found to work together in order to prevent oxidation of telomeric DNA at chromosome ends- which could be used to effectively turn off cancer’s immortality, letting it die slowly and naturally.
Among the targets in cancer treatment is that the enzyme telomerase. Usually, telomerase prevents telomeres from shortening in stem and germ cells, which assists with growth. However, telomerase can also be highly effective in cancer cells, so maintaining their telomeres undamaged a
nd producing the cells almost immortal.The new work proves that interrupting PRDX1 and MTH1 prevents telomerase from counteracting telomere shortening. Thus far, attempts to block telomerase in cancer have never been fruitful at the practice. The discovery of these co-operating enzymes opens up a fresh chance to block telomerase.
“Instead of inhibiting the enzyme itself, we target its substrate – the chromosome end – making it un-extendable by telomerase,” says Lingner.
