The Impact of the Serotonin on the Cause and Treatment of Cancer

What is it about?

This review article goes through many researches based on the effectiveness of the neurotransmitter serotonin on cancer cells and also the impact of SSRIs (selective serotonin reuptake inhibitors) drugs on the cause of certain types of cancers. Serotonin has been shown to be a mutagenic factor for a wide range of normal and tumor cells. Serotonin exhibits a growth stimulatory effect in aggressive cancers and carcinoids usually through 5- HT1 and 5-HT2 receptors. In contrast, low doses of serotonin can inhibit tumor growth via the decrease of blood supply to the tumor, suggesting that the role of serotonin on tumor growth is concentration-dependent. Serum serotonin level was found to be suitable for prognosis evaluation of urothelial carcinoma in the urinary bladder, adenocarcinoma of the prostate and renal cell carcinoma.The mechanism that connect serotonin with tumor evolution seem to be related to the serotonin impact on tumor associated macrophages.

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Why is it important?

SSRIs may lead to both tumor progression and tumor inhibition via two different mechanisms and it is a matter of luck and probably tumor type regarding which of the mechanism will dominate. If the immune system is already suppressed due to chemo or other reasons, using SSRIs may help. If the immune system is in a good shape, SSRIs would better to be avoided. Chloroquine may also have immunosuppressive activity. Next to its serious anti-cancer potential, there may also be a negative impact on the immune system. Some of the best ways to address the influence of serotonin in cancer is via the inhibition of 5-HT receptors over expressed in many tumor types and not via the inhibition of serotonin transporter. From a 5-HTR inhibition point of view; we would probably suggest the use of Cyproheptadine in combination with Propranolol. These should address both 5-HT-1 and 5-HT-2 receptors, which seem to be the most relevant in most cancers. Serotonin was shown to suppress MMP-12 production in tumor associated macrophages and as a result inhibit the generation of angiostatin. Conversely, the inhibition of serotonin leads to angiostatin production which reduces tumor growth due to angiostatin’s angiogenesis inhibition activity. Therefore, this effect is related to the tumor associated macrophages. serotonin directly impacts on cell growth via binding to its receptors. The 5-HT-1 and 5-HT-2 receptors are extensively expressed in the human breast cancer, prostate cancer, bladder cancer cells and other cancer types. Serotonin direct impact on vessels per fusing the tumor and Intra-vital microscopy studies have also shown that vessels per fusing the tumor exhibit a specific vasconstrictive response to 5HT1 agonists. In line with the above, during tumor progression, tyrosine hydroxylase, the rate-limiting enzyme in the serotonin biosynthesis pathway, is often up-regulated.

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