In 2003, scientists completed mapping the human genome and discovered that less than 2 percent of our approximately 20,000 genes code for proteins. What purpose is served by all the other genes, the non-coding DNA dubbed “junk DNA?" New research from British and American scientists suggests at least some of our non-coding DNA may be essential to disabling disease within our bodies.

Their new study has identified a strand of non-coding RNA — transcribed from a stretch of junk DNA — that prevents cells from turning cancerous.

Within each of our cells, RNA acts as the helping hand of DNA by ferrying the genetic code needed to create proteins around the cell. RNA is made of nucleotides formed into a single strand, while DNA is similarly constructed from nucleotides formed into double strands. Long noncoding RNA (lncRNA), which do not encode proteins and constitute lengths of more than 200 nucleotides, are known to play a role in gene regulation both during our development and during disease formation, the researchers explain in their introduction to the study.

Based on this knowledge, Dr. Adele Murrell, lead author of the study and a cancer researcher at University of Bath, focused on lncRNA in the investigation of breast cancer.

Underlying Genetics of Cancer

Cancer begins when the cells replacing those that die begin to outnumber their predecessors. As Murrell explains, the control switch (which is genetic) gets stuck in the ‘on’ position. As a tumor grows, cancer cells begin to break away, change shape, and burrow through tissues to the bloodstream where they migrate to other parts of the body. Spreading cancer is called metastasis, a process that requires “a whole network of genes to regulate the transformation of cell shape and mobilization,” Murrell stated in a press release.

Looking at a region of the genome that is often damaged in breast cancer patients, Murrell and her colleagues singled out a strand of lncRNA, known as GNG12-AS1. To study GNG12-AS1 and its effects, the research team decided to use smaller interfering RNAs to either stop it from being made or to degrade it immediately after it was formed. Both experiments led to cells changing their shape and transforming into migratory cells — cancer metastasis occurred whenever GNG12-AS1 was silenced.

When this lncRNA is working correctly, it performs two separate functions that help maintain healthy cells, the researchers say. First it regulates the levels of a neighboring gene involved in cell replication, and second, it suppresses the network of genes involved in metastasis.

Ultimately, any new information gleaned from this study should contribute to the development of innovative cancer treatments, the team says. A fruitful search among junk DNA yielded an unfound gem.

Source: Stojic L, Niemczyk M, Orjalo A, et al. Transcriptional silencing of long noncoding RNA GNG12-AS1 uncouples its transcriptional and product-related functions. Nature Communications. 2016.