Junk DNA May Enhance Cancer Protection
Research could lead to the development of new cancer treatments.
Researchers have discovered that the DNA found in between genes actually has a role in suppressing cancer in a recent study.
Human genomes were previously found to have approximately 3 meters of DNA, with only 2% that are able to code for proteins. It has been unclear what role the other 98% serves.
Non-coding RNAs are difficult to knockout without causing any damage to the DNA. If the DNA is damaged it can lead to false results and off target effects.
A recent discovery published in Nature Communications was able to identify a piece of non-coding RNA that is able to stop cells from turning cancerous.
"Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place,” said researcher Kat Arney.
The hope is that these findings lead to the development of new cancer treatments.
“The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die,” said lead researcher, Adele Murrell. “Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumor grows and the cancer cells get crowded, they start to break away from the tumor, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilization.”
During the study, researchers found these non-coding RNA fragments are able to maintain healthy cells. This can be accomplished by regulating the levels of DIRAS3, a neighboring gene involved in cell replication. Another method to accomplish this is through suppressing a network of genes that prep cells to be able to change shape and prepare for metastasis.
In order to differentiate between the 2 mechanisms, researchers used smaller interfering RNAs (siRNAs) to stop the non-coding RNAs from being made, or to degrade the RNA immediately after it is made.
Although both of these methods allowed for the cells to change shape and transform into migratory cells, only the first method affected DIRAS3 and the cell cycle.
"In our study we've identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis,” Dr. Murrell said. “The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread."