Blocking a single protein inside cells could dramatically slow colorectal cancer, scientists claim.
Researchers in South Korea found that shutting down a gene called NSMF, which makes a protein that helps cancer cells cope with rapid cell division, caused tumors to suffer from 'irreversible cellular aging.'
Normally, cancer cells divide rapidly, with NSMF inducing DNA damage and the emergence of new mutations.
But the scientists found that when they stopped the gene from functioning in lab and mouse experiments, tumor growth slowed or stopped completely.
In the mouse experiments, removing NSMF led to significantly fewer intestinal growths. The animals also lived 33.5 percent longer on average than those that still had the gene.
Researchers also found no noticeable damage to healthy intestinal cells in mice, suggesting that shutting off the gene could target tumors without damaging other cells, unlike chemotherapy, which can attack non-cancerous cells.
The findings come as colorectal cancer is rising sharply among young adults. Cases among Americans under 50 have roughly doubled since the mid-1990s, as more people experience subtle symptoms that are often dismissed or misdiagnosed.
On February 11, Dawson's Creek actor James Van Der Beek died from the cancer at 48 years old. The actor reportedly dismissed the early warning signs, blaming the change in his bowel movements on his morning coffee instead of the disease.
He was diagnosed with stage three colorectal cancer in 2023, in his mid 40s, and went through near-constant doctors appointments and painful treatments that rendered him unable to work.
Researchers behind the new study believe that while more research is needed in humans, they could eventually led to new treatments that boost survival.
Dr Kyeong Jin Shin, a cancer expert at the Ulsan National Institute of Science and Technology (UNIST), who led the study, said: 'Our findings suggest that NSMF is a promising... target.'
'By inducing a state of permanent aging in cancer cells, we can effectively stop tumor growth without harming normal tissues.'
He added that developing drugs to block the protein 'could offer a novel treatment approach' against the cancer.
In the study, published in the journal Nucleic Acids Research, researchers blocked the protein from NSMF using antibodies in the lab experiments or, in the mouse experiments, by breeding a strain of mice that did not have the gene.
It is not clear by how much blocking NSMF slowed the growth of colorectal cancer tumor cells.
The researchers also did not suggest in their study how the NSMF gene could be blocked in humans.
In the study, researchers analyzed NSMF, also called N-methyl-D-aspartate receptor synaptonuclear signaling and neuronal migration factor (NSMF).
Researchers in South Korea made the breakthrough via lab and mouse experiments.
In lab experiments, the scientists used antibodies to block the NSMF-made protein in human colorectal cancer cells and monitored the effects.
In a separate experiment, they bred mice that did not have NSMF with others that had a higher risk of developing intestinal tumors.
The offspring were then tracked for up to 16 to 20 weeks, before their intestinal tissue was examined for cancer growth.
Researchers said that while blocking NSMF reduced tumor growth, it did not completely eliminate the cancer.
At this stage, it was not clear how the gene might be turned off safely in humans, but researchers said their study was a promising first step to a potential treatment.
Professor Young Chan Chae of the Department of Biological Sciences at UNIST, who led the study, said: 'This research uncovers a previously unknown role for NSMF in colorectal cancer.'
'Developing inhibitors against this protein could offer a novel treatment approach that causes cancer cells to naturally age and die, providing a potential new avenue for therapy.'