Cell division is a crucial process in the body, but cancer cranks it into overdrive with often deadly results. Now, researchers from the University of Copenhagen have identified a protein that plays a key role in the process, meaning it could be a future treatment target for a range of cancer types.
Cell division has two distinct phases. During the first, known as S-phase, a cell’s DNA duplicates completely. Then mitosis follows, where the cell splits in two, with each new cell getting a full copy of the original DNA.
But a few years ago a new step in the process was discovered. If S-phase doesn’t go as planned, a cell can instead duplicate its DNA through mitotic DNA synthesis (MiDAS), in preparation for splitting.
Most of the time, healthy cells don’t bother with MiDAS – S-phase is usually neat enough already. But cancer was found to make heavy use of MiDAS, due to being under a lot of replication stress during its S-phase.
That makes it an attractive target for cancer treatments. After all, if MiDAS is interrupted, the cell will die.
So for the new study, the Copenhagen researchers set out to investigate MiDAS further. Experimenting with bone, cervical and colon cancer cells, they monitored which proteins play a part in MiDAS. And one in particular, named RTEL1, caught their attention as a promoter of the process.
“We believe that this RTEL1 function is critical for any cancer cells that rely on MiDAS, which is more than 80 percent of the known cancer types based on our knowledge,” says Ying Liu, co-lead author of the study. “Therefore, we can use this to design drugs to inhibit RTEL1 and hopefully selectively kill cancer cells.”
There is a complicating factor though – the team also found that RTEL1 plays an equally important role in the division of healthy cells, preventing DNA damage and chromosome instability during the S-phase.
The team says that future work will investigate the two roles of this protein and whether they’re related. And by studying how RTEL1 promotes mitosis in cancer cells, new clues may arise to focus on just cancer instead of healthy cells.
The research was published in the journal Nature Structural & Molecular Biology.
Source: University of Copenhagen
