Presentation: 2025 ND EPSCoR Annual conference 

October 21, 2025, NDSU Memorial Union, Fargo, North Dakota

Serotonin as a target modulator of cell migration in breast cancer cells

Cell migration requires a delicate balance of cellular adhesion to the extracellular matrix (ECM). Focal adhesion complexes are responsible for this balance. In the context of breast cancer, dysregulation of such adhesions contributes to disease progression and metastasis. Recently, the serotonergic signaling network has become a target of interest in breast cancer progression. Increases in serotonin result in increased cell survival, invasion, and proliferation in breast cancer cells, yet the underlying mechanisms of its tumor-promoting properties are poorly understood. Serotonin plays a key role in maintaining mammary epithelium homeostasis evidenced by the expression of both the rate-limiting enzyme in its biosynthesis, tryptophan hydroxylase, and various serotonin binding sites such as serotonin receptors and the serotonin transporter. Peripherally produced in enterochromaffin cells, serotonin is stored in the cytoplasm of platelets. Upon activation, platelets aggregate, secreting serotonin in the process. Among other factors, serotonin has been suggested to influence platelet aggregation through its transamidation to Rho GTPases, a process known as serotonylation. Rho GTPases modulate focal adhesion dynamics, which ultimately influence cell migration. As abnormal cell migration is the fundamental issue of breast cancer progression and metastasis, we aim to investigate the role that serotonin plays in cell migration. In order to address this question, we have treated breast epithelial cell lines with serotonin and transforming growth factor beta (tgfB). Given that tgfB treatment induces metastatic-like characteristics in normal breast epithelial cells, we expect to see similarities in the characterization of focal adhesion complexes between both treatments.