Blocking enzymes could make cancer cells mortal

Scientists have found two specific antioxidant enzymes that are linked to making cancer cells mortal. According to a study conducted by the Ecole Polytechnique Fédérale De Lausanne, PRDX1 and MTH1 have the ability to shun the cancer cells completely. Before cell division, the long strings of the cell's DNA are wrapped tightly into the structures known as chromosomes. This protects the cell's genetic material from physical and chemical damage. The ends of chromosomes are called telomeres. These are specialised structures that have to be replicated with each cell division cycle. But the complete replication of telomeres up to the very ends of chromosomes also requires specialised mechanisms, and these are limited. Telomeres are also very sensitive to oxidative damage, which affects their ability to replicate. Because of this, telomeres shrink over time, limiting the lifespan of cells. Telomere shortening is essentially the cause of cell aging. Now, researchers have discovered the two antioxidant enzymes - PRDX1 and MTH1 - that work together to prevent oxidation of telomeric DNA at chromosome ends. The scientists disrupted both the enzymes in cancer cells and found that the cells' telomeres shrunk with every round of cell division, eventually disappearing altogether. One of the promising targets in cancer therapy is the enzyme telomerase. Normally, telomerase prevents telomeres from shortening in germ and stem cells, which helps with development. But telomerase is also highly active in cancer cells, keeping their telomeres intact and making the cells virtually immortal. The new work shows that disrupting PRDX1 and MTH1 prevents telomerase from counteracting telomere shortening.  So far, attempts to efficiently block telomerase in cancer have not been fruitful in the clinic. The study appears in the journal Genes & Development.

Decoded: How melatonin promotes sleep 

Researchers have found that the melatonin hormone promotes sleep by suppressing the neurons responsible for keeping us awake, a discovery that may lead to new therapy for insomnia. "We as a society are losing sleep because we are working too hard, and it's causing a variety of health concerns," says an expert. In a study, published in Journal of Pineal Research, a research team used a mouse model and found that when melatonin is infused in the brain of an awake and active mouse at dark, it increased sleep and reduced its activeness by suppressing certain specific neurons that stimulate the brain to stay awake. It also showed that blocking melatonin receptors in the brain during bedtime, increased wakefulness. The experiments focused on a receptor, MT1, as the mechanism using which melatonin acts to inhibit the specific orexin neurons that wake you up. This discovery may also help developing medications that target only the MT1 receptor instead of multiple receptors, which could lead to fewer side effects for those who take sleep-promoting drugs. Melatonin has been used as a sleep drug for many years, but people didn't know how it worked.    — Agencies