Researchers Uncovered How “Junk” DNA Can Lead To The Development And Progression Of Cancer, And This Is A Discovery That Paves The Way For Innovative Treatment Options
Scientists have previously found that non-coding and repetitive DNA patterns– also known as “junk” DNA– can be disruptive to the repair and replication of our genome.
But, a new study conducted by researchers at The Institute of Cancer Research in London (ICR) has finally uncovered just how this phenomenon can contribute to the development of cancer.
The scientists first recreated the process of DNA replication within a test tube. Then, they analyzed exactly how repetitive DNA patterns are copied during the replication process.
The team realized that “junk” DNA is actually able to stall replication completely– leading to an increased margin of error that can be an early contributing factor to the development of cancer.
More specifically, the researchers found that when repetitive DNA was encountered during DNA replication, its DNA strands were unwound– but there was sometimes failure to copy the opposite DNA helix strand.
And unfortunately, this error can cause all replication to halt.
This discovery has led the researchers to believe that repetitive DNA sequences might trigger a damage response signal which indicates that the genome requires repair.
Genome instability and DNA damage are both known drivers that promote the formation and progression of cancer.
So, this research underscored a relationship between junk DNA and cancer.
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“This study helped unravel the puzzle of junk DNA– showing how these repetitive sequences can block DNA replication and repair,” explained Kristian Helin, the Chief Executive of ICR.
“It’s possible that this mechanism could play a role in the development of cancer as a cause of genetic instability– especially as cancer cells start dividing more quickly and place the process of DNA replication under more stress.”
Now equipped with these DNA replication findings, the researchers hope their improved understanding will lead to new cancer treatment options.
“Understanding the mechanisms underlying genetic mutation and instability is critical if we are to find innovative new ways to treat cancer that exploit fundamental weaknesses in cancer cells,” Helin added.
To read the study’s complete findings which have since been published in Nature Communications, visit the link here.
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