Scientists have made a groundbreaking discovery that could change the way we understand and treat cancer. A team of researchers has found that an RNA molecule, known as NEAT1, plays a crucial role in repairing damaged DNA. This finding could lead to new therapies that target tumors with high NEAT1 expression, offering fresh hope for cancer patients.
Our DNA is constantly at risk. Every time a cell divides, errors can occur in the genetic code. External factors such as sunlight, alcohol, and cigarette smoke also damage DNA over time, increasing the risk of cancer and other diseases.
Fortunately, our cells have a built-in defense system called the DNA damage response (DDR). This system detects and repairs broken DNA strands, ensuring the stability of our genetic code. Until now, scientists have primarily focused on proteins in this repair process. However, a new study has revealed that RNA, specifically the long non-coding RNA called NEAT1, plays a key role in maintaining genome stability.
The Discovery of NEAT1’s Role
A research team from Julius-Maximilians-Universität Würzburg (JMU) in Germany has found that NEAT1 helps cells recognize and repair broken DNA. The study, led by Dr. Kaspar Burger from the Department of Biochemistry and Molecular Biology, was published in Genes & Development.
“In our study, we focused on long non-coding RNA transcripts. Previous data suggested that some of these transcripts act as regulators of genome stability. We were able to show that DNA double-strand breaks increase both the number of NEAT1 transcripts and the amount of N6-methyladenosine marks on NEAT1,” said Dr. Burger
NEAT1 is found in high concentrations in many tumor cells and reacts to DNA damage and cellular stress. However, its precise role in DNA repair was previously unclear. The research team discovered that when DNA breaks occur, NEAT1 undergoes a chemical modification known as methylation, which helps the cell recognize damaged DNA more efficiently.
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How NEAT1 Helps Repair DNA
The experiments showed that highly methylated NEAT1 accumulates at sites of DNA damage, allowing the cell to quickly identify and respond to the problem. When researchers suppressed NEAT1 in cancer cells, the DNA damage response was delayed, leading to more DNA damage.
NEAT1 itself does not directly repair DNA, but it helps release and activate an RNA-binding DNA repair factor. “This process enables the cell to recognize and repair DNA damage much more efficiently,” explained Dr. Burger.
A New Approach to Cancer Treatment?
The discovery of NEAT1’s role in DNA repair opens new possibilities for cancer treatment. Scientists believe that targeting NEAT1 could be a potential strategy for treating tumors with high NEAT1 expression. However, more research is needed to determine whether these findings in cell models can be applied to real cancer cases.
Dr. Burger said, “This study represents a major step in understanding the role of RNA in DNA repair. If we can confirm these results in complex tumor models, it could lead to new therapeutic strategies for cancer patients.”