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Study From China: New Antidepressant Shows Promise for Cancer Treatment

On January 23, 2024, a study from China attracted global attention. Scientists have discovered a new type of antidepressant, amsofaxine hydrochloride, which not only relieves depression, but also enhances the body’s resistance to certain types of cancer.

In this study, researchers combined amsofaxine hydrochloride with an anti-tumor drug and found that it inhibited the growth of colon cancer cells in cell culture and mouse experiments while strengthening the immune system, triggering a A phenomenon called “programmed cell death.” Although this discovery has not yet been tested in humans, the potential for this result to be used as an actual cancer treatment is still worth looking forward to.

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It is worth mentioning that researchers found that amsofaxine hydrochloride can enhance the immune response of so-called “CD8+T” cells in mice. These cells are the most powerful executors of anti-cancer immune responses. In addition, the mice in the experiment had an increased proportion of natural killer cells and macrophages in the spleen and tumors, effectively inhibiting the growth of cancer.

When the researchers used amsofaxine and cancer immunotherapy together in mice, they managed to completely eliminate tumors from 20% of the samples, creating long-term immunity. “Our work suggests that combined use with amsufaxine hydrochloride may be a promising cancer treatment,” the research team concluded.

Antidepressant drugs affect cancer cell metabolism pathways

Advertisement (Please continue reading this article) (A) Representative images of tumor-free mice after rechallenge. (B, C) Tumor growth curves of tumor-free (T-free) and untreated (naïve) mice (n = 4). “Rechallenge” here usually refers to experiments in which mice that have been previously treated and have no tumors are again injected or exposed to conditions that can induce tumors to test their immune response or tumor resistance. Part (A) of the figure shows images of these mice, while parts (B) and © show tumor growth in these mice compared with untreated mice (i.e., mice that have not been exposed to tumors). Compare the curves. These data are important for evaluating treatment efficacy and understanding tumor immunology.

What makes amsofaxine hydrochloride different from other antidepressants is its triple action against depression: not only does it inhibit the reuptake of serotonin, it also slows the reuptake of norepinephrine and dopamine. There is evidence that depression and other forms of psychological stress are risk factors for promoting cancer growth, likely by suppressing the immune response, but whether antidepressants can help combat this risk is difficult to determine.

Additionally, in 2021, an older antidepressant drug, a monoamine oxidase inhibitor, was also found to enhance the immune response to cancer in mice. Importantly, antidepressants do not appear to be effective alone in fighting cancer. They need to be combined with anti-cancer drugs that prevent tumors from evading the body’s immune system. Once the immune system can recognize cancerous tissue, using antidepressants appears to produce more molecules that are toxic to cancer cells.

This line of research is still in its infancy, but preliminary research suggests that antidepressants can enhance the effects of cancer drugs by affecting the metabolic pathways of cancer cells, although other studies tentatively suggest that antidepressant use may actually Cause cancer. Until more research is done, it is difficult to draw concrete conclusions in clinical practice.

The research has been published in Frontiers in Pharmacology.

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First image source: Shutterstock/Kateryna Kon cc By4.0

Image Source:Frontiers in Pharmacologycc By4.0

Reference papers:

1.Mutations associated with autism lead to similar synaptic and behavioral alterations in both sexes of male and female mouse brain. Frontiers in Pharmacology

Further reading:

1.“I want to be a good person” makes bad cells good: using phagocytosis to fight cancer

2024-01-24 04:07:28

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