Serotonin is often called the happy chemical because of its well-known role in mood regulation.
however,
recent studies suggests that this familiar molecule may play an unexpected role in cancer development. Not through an effect on the brain, but through a completely different mechanism in other parts of the body.
Although serotonin is commonly associated with the brain,
almost 95 percent serotonin in the body is produced in the intestines.
From there, it enters the bloodstream and travels to various organs and tissues, including the liver, pancreas, muscles, bones, fat tissue, and immune cells.
Gut serotonin helps regulates blood sugar levels by acting on the liver and pancreas and regulates body temperature by acting on adipose tissue.
It also helps maintain bone health, stimulate appetite and bowel movements, enhance sexual health, promote wound healing, and support immunity against harmful microbes.
It essentially controls the functions of many cells throughout the body, and its effects extend far beyond mood regulation.
In 2019, scientists at the Icahn School of Medicine at Mount Sinai in New York
revealed that serotonin can enter cells and interact directly with DNA.
They found that it binds to molecular “switches” that control whether genes are active or inactive – and this binding can turn on specific genes.
Since then, research has shown that serotonin can turn on genes involved in the growth of cancer. This mechanism has been seen in brain, liver and pancreatic cancers – and it may play a role in many other cancers.
My colleagues and I are currently at the University of Limerick in Ireland
investigating interaction between serotonin and DNA to better understand how it affects cancer.
Identifying the specific sites where serotonin binds to cancer-related genes could support the development of targeted “epigenetic” therapies — treatments that control which genes are turned on and off.
Epigenetic therapy aims to reprogram cancer cells by directly adjusting their gene activity. They can specifically turn off harmful genes and turn on helpful ones in cancer cells without changing the DNA sequence itself.
Such therapy may one day attack cancer cells with greater precision than current methods: surgery, chemotherapy and radiotherapy. (Although these approaches can save lives, they are often aggressive, have significant side effects, and do not always prevent relapse.)
Scientists are also investigating how serotonin, produced in the gut, reaches cancer cells.
Understanding this pathway may allow doctors to manage serotonin levels in patients.
Approaches may include dietary changes, maintaining a healthy gut microbiome, or using antidepressants called “selective serotonin reuptake inhibitors” (SSRIs).
Cells take up serotonin through tiny “transport channels,” and SSRIs block these channels, limiting the flow of serotonin into cancer cells.
These drugs increase serotonin levels in the body, but prevent it from reaching DNA to cause cancer. This strategy can complement existing treatments and possibly increase their effectiveness.
Unraveling the double life of serotonin
Brain and gut serotonin work largely independently. Serotonin, which affects mood, does not appear to promote cancer growth.
For example, in people with depression, serotonin activity in the brain may be lower, but serotonin produced in the gut does not seem to have
clear effect on brain serotonin.
SSRI antidepressants like Prozac, Celexa, and Zoloft increase serotonin levels in the brain, so people who take these pills don’t have to worry about their pills causing cancer.
On the contrary, as mentioned above,
early studies suggest that SSRIs may have a beneficial effect on some cancers – although larger clinical trials are needed to confirm this.
Our research aims to gain a detailed understanding of the role of serotonin in various tissues and cellular pathways, potentially opening up new opportunities for treatment.
However, significant challenges remain.
A better understanding of how serotonin interacts with cancer-related genes is needed to determine which targets are most effective. Precise delivery systems must also be developed to ensure that epigenetic drugs reach their intended sites of action.
Most importantly, promising results from cellular experiments must be confirmed in ethically designed animal studies and human clinical trials before significant progress can be claimed.
If a therapy can be developed that targets serotonin activity specifically in cancer cells, tumors will become less aggressive and easier to remove surgically, with less risk of recurrence.
A fuller understanding of serotonin’s functions in the body—through mood, metabolism, and cancer—may guide the development of more precise and effective treatments in the future.
Also watch:
PhD Student, Virus and Cancer Genes, University of Limerick
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