'Junk' DNA could lead to cancer by stopping copying of DNA


Non-coding DNA, also known as "junk DNA," has been discovered to be anything but harmless and inactive and may even play a role in the onset of cancer.

Research has demonstrated how non-coding DNA might obstruct our genome's replication and repair processes, potentially causing mutations to build up.

It has been discovered before that non-coding or repetitive DNA sequences, which make up around half of our genome, can obstruct genome replication.

However, scientists do not yet fully comprehend the underlying mechanism or how it can influence the onset of cancer. In order to better comprehend DNA replication, researchers at The Institute of Cancer Research, London, recreated the entire process in a test tube for the new study.

The scientists were able to explain how repetitive DNA patterns can completely block DNA replication and increase the likelihood of mistakes, which can act as a precursor to cancer. This important information could eventually result in improved medications and therapies.

The findings, in the opinion of the researchers, may also aid in improving the diagnosis and follow-up of some tumors, such as bowel cancer, where frequent faults in the replication of repetitive DNA sequences signal whether cancer is advancing.

The Institute of Cancer Research (ICR) provided further support for the study, which was supported by Wellcome and the Royal Society and published in Nature Communications.

Researchers at the ICR, a nonprofit research and educational organization, discovered that the DNA replication mechanism could unwind repetitive DNA strands but occasionally failed to replicate the opposite DNA strand. The replication mechanism may fail as a result of this error, much like how DNA damage causes the replication process to collapse.

According to the research, repeated DNA patterns can cause a damage response signal, which would indicate that errors in DNA replication have occurred and need to be fixed.

The study further supports the association between junk DNA and cancer, which is known to increase cancer formation and progression due to DNA damage and the resulting genome instability.

The first concrete proof that DNA damage is the underlying cause of cancer was offered in the 1960s by researchers at the ICR. ICR researchers later shown that tumors with DNA repair defects may be genetically targeted with medications known as PARP inhibitors in the early 2000s.

Now, our experts are hoping that a better comprehension of DNA replication and how it might go awry will result in novel strategies to treat the condition.

Team head in genome replication at The Institute of Cancer Research in London and study author Dr. Gideon Coster said:

"We were interested in discovering why cells appear to have a harder time copying repeated DNA sequences than other regions of the genome. According to our research, so-called junk DNA actually plays a significant and potentially harmful role in cells by preventing DNA replication and posing a risk for malignant mutations.

"The response brought on by repetitive DNA sequences is now thought to be very similar to the reaction brought on by DNA damage, which is known to cause cancer. Therefore, our study significantly broadens our understanding of cancer, and I'm optimistic that it may someday lead to the development of novel therapies."

The Institute of Cancer Research's Chief Executive Officer, Professor Kristian Helin, stated:

"This research contributes to the understanding of junk DNA by demonstrating how these repetitive patterns can prevent DNA replication and repair. It's probable that this mechanism, which results in genetic instability, contributes to the emergence of cancer. This is especially true given that cancer cells begin to divide more quickly, which puts the process of DNA replication under additional strain.

Understanding the mechanisms underlying genomic instability and mutation is essential if we are to develop novel cancer treatments that take advantage of inherent flaws in cancer cells.