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Updated: Oct 16, 2025

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
Published on: March 17, 2016
Serotonin after β-Adrenoreceptors' Exposition: New Approaches for Personalized Data in Breast Cancer Cells
Ana Salomé Correia1,2, Diana Duarte1,3, Isabel Silva4
1OncoPharma Research Group, Center for Health Technology and Services Research (CINTESIS), Rua Dr. Plácido da Costa, 4200-450 Porto, Portugal.
Abstract:
Serotonin is an important monoamine in the human body, playing crucial roles, such as a neurotransmitter in the central nervous system. Previously, our group reported that β-adrenergic drugs (ICI 118,551, isoprenaline, and propranolol) influence the proliferation of breast cancer cells (MCF-7 cells) and their inherent production of adrenaline. Thus, we aimed to investigate the production of serotonin in MCF-7 cells, clarifying if there is a relationship between this production and the viability of the cells. To address this question, briefly, we treated the MCF-7 cells with ICI 118,551, isoprenaline, and propranolol, and evaluated cellular viability and serotonin production by using MTT, Sulforhodamine B (SRB) and Neutral Red (NR) assays, and HPLC-ECD analysis, respectively. Our results demonstrate that isoprenaline promotes the most pronounced endogenous synthesis of serotonin, about 3.5-fold greater than control cells. Propranolol treatment also increased the synthesis of serotonin (when compared to control). On the other hand, treatment with the drug ICI 118,551 promoted a lower endogenous synthesis of serotonin, about 1.1-fold less than what was observed in the control. Together, these results reveal that MCF-7 cells can produce serotonin, and the drugs propranolol, isoprenaline and ICI 118,551 influence this endogenous production. For the first time, after modulation of the β-adrenergic system, a pronounced cellular growth can be related to higher consumption of serotonin by the cells, resulting in decreased levels of serotonin in cell media, indicative of the importance of serotonin in the growth of MCF-7 cells.
Insights
This study shows that breast cancer cells (MCF-7) produce serotonin. Beta-adrenergic drugs like isoprenaline and propranolol significantly increase serotonin production, impacting cell viability and growth.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Serotonin is a key neurotransmitter with diverse physiological roles.
- Previous research indicated beta-adrenergic drugs affect breast cancer cell proliferation and adrenaline production.
- The role of serotonin production in MCF-7 cell viability remained unclear.
Purpose of the Study:
- To investigate serotonin production in MCF-7 breast cancer cells.
- To determine the relationship between serotonin production and MCF-7 cell viability.
- To examine the influence of specific beta-adrenergic drugs on serotonin synthesis.
Main Methods:
- MCF-7 cells were treated with beta-adrenergic drugs: ICI 118,551, isoprenaline, and propranolol.
- Cellular viability was assessed using MTT, Sulforhodamine B (SRB), and Neutral Red (NR) assays.
- Serotonin production was quantified using High-Performance Liquid Chromatography with Electrochemical Detection (HPLC-ECD).
Main Results:
- Isoprenaline significantly increased endogenous serotonin synthesis by approximately 3.5-fold compared to controls.
- Propranolol treatment also enhanced serotonin synthesis relative to control conditions.
- ICI 118,551 treatment resulted in a slight decrease in endogenous serotonin synthesis (approx. 1.1-fold less than control).
- A correlation was observed between pronounced cellular growth and increased serotonin consumption, indicated by decreased media serotonin levels.
Conclusions:
- MCF-7 cells are capable of endogenous serotonin production.
- Beta-adrenergic drugs (propranolol, isoprenaline, ICI 118,551) modulate serotonin production in these cells.
- This study provides the first evidence linking beta-adrenergic system modulation, altered serotonin levels, and breast cancer cell growth, highlighting serotonin's importance in MCF-7 cell proliferation.
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