Washington D.C. [USA], Oct 22 (ANI): A team of researchers has recently found a "suicide molecule" that forces tumours to self-destruct and trigger a fail-safe mechanism that may protect us from cancer.
Small RNA molecules originally developed as a tool to study gene function trigger a mechanism hidden in every cell that forces the cell to commit suicide, reports a study, the first to identify molecules to trigger a fail-safe mechanism that may protect us from cancer.
"It's like committing suicide by stabbing yourself, shooting yourself and jumping off a building all at the same time," said lead study author Marcus Peter.
He has been searching for the phantom molecules with this activity for eight years.
This study describes the discovery of the assassin molecules present in multiple human genes and their powerful effect on cancer in mice.
Thus began his search for natural molecules coded in the genome that kill cancer.
But he found them by testing a class of small RNAs, called small interfering (si)RNAs, scientists use to suppress gene activity.
siRNAs are designed by taking short sequences of the gene to be targeted and converting them into double- stranded RNA. These siRNAs when introduced into cells suppress the expression of the gene they are derived from.
Peter found that a large number of these small RNAs derived from certain genes did not, as expected, only suppress the gene they were designed against. They also killed all cancer cells.
His team discovered these special sequences are distributed throughout the human genome, embedded in multiple genes as shown in the study in Cell Cycle.
To test this in a treatment situation, Peter collaborated with Dr Shad Thaxton, associate professor of urology at Feinberg, to deliver the assassin molecules via nanoparticles to mice bearing human ovarian cancer.
In the treated mice, the treatment strongly reduced the tumor growth with no toxicity to the mice, reports the study in Oncotarget.
Importantly, the tumors did not develop resistance to this form of cancer treatment.
"The problem is cancer cells are so diverse that even though the drugs, designed to target single cancer driving genes, often initially are effective, they eventually stop working and patients succumb to the disease," Peter stated.
The research appears in eLife journal. (ANI)