Scientists Discover Fungi That Can Stop Cancer to Live Longer

Some long-lived fungi species appear to be able to use a special type of cell division to stop cell mutations in their tracks, reducing the chances of cancers growing, scientists have discovered.

Fungi are comprised of networks of filaments known as mycelium. Within the cells of these filaments, there are usually single nuclei with half a set of chromosomes, known as "haploid," similar to a human sperm or egg. Only when the fungus needs to produce spores to reproduce asexually, such as in the gills of mushrooms do these nuclei fuse.

Researchers from Wageningen University & Research revealed in a paper published in the journal Microbiology and Molecular Biology Reviews that mutations may arise in these nuclei that prevent the mycelium filaments from fusing, therefore stopping the fungus's ability to produce spores and reproduce asexually.

These mutant nuclei are therefore a fungal parallel of cancers in humans and plants: robbing their host for their own uncontrolled growth.

"Mutations can occur in fungal mycelia—the below-ground network of fungal filaments—that give the nucleus a competitive advantage in the mycelium," Duur Aanen, co-author of the paper and researcher at Wageningen University & Research, said in a statement. "Because these mutations are selected within the mycelium, but reduce the fitness of the mycelium as a whole, you can think of them as a kind of 'nucleus cancers.'"

However, the researchers found that some fungi can avoid these mutations and therefore live extremely long via using a special type of cell division called a "clamp connection" to prevent the accumulation of damaging mutations. This involves the nuclei being held in a separate compartment to check for their genetic quality before fusion is allowed to proceed.

Newsweek reached out to the authors of the study via email for comment.

"Both nuclei [are] continuously testing each other for the ability to fuse, a test that nuclei with mutations in fusion genes fail," Aanen said. "If the cell cannot fuse, it means a dead-end for the cell and thus the end of its nucleus."

"My colleagues and I have now proposed a new hypothesis: that the fusion of the clamp connection is a test moment for one of the haploid nuclei. Since our previous research revealed that loss of fusion is the main route to nucleus cancers, we hypothesized that the clamp connection acts as a screening device for the quality of the nucleus, with both nuclei continuously testing each other for the ability to fuse, a test that nuclei with mutations in fusion genes fail. We therefore argue that mycelia have a constant and low risk of nucleus cancers, regardless of their size and lifespan."

This mechanism is only found in longer-lived fungal species, as those with short lifespans have no need to prevent these "cancers" from arising.

This is another example of organisms evolving mechanisms to avoid the accumulation of cancerous mutations in order to live long lives.

As an organism proceeds through its life, it usually gains increasing numbers of mutations that harm it, which may lead one to expect that a longer-lived organism is more riddled with cancer. However, there is very little variation in lifetime-cancer risk between animal species, a finding known as Peto's paradox. Animals like elephants and whales defy this logic by having evolved ways to reduce their cancer risk and keeping DNA mutations in check.

Fungi, it seems, are capable of doing the same.

"By linking differences in longevity of the mycelial phase to ecology and stringency of nuclear quality checks, we propose that mycelia have a constant and low lifetime cheating risk, irrespective of their size and longevity," the authors wrote.

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