University Archives

Minoxidil, a potassium channel opener first introduced as an antihypertensive, is now widely prescribed to stimulate hair growth. In oncology, it has gained increasing use as a supportive therapy for breast cancer patients experiencing alopecia induced by chemotherapy or endocrine treatments such as Tamoxifen. Although Minoxidil is widely used, its molecular activity in hormone-responsive cells remains unclear. Because it has been shown to influence androgen receptor signaling, we aim to determine whether Minoxidil similarly impacts the estrogen–estrogen receptor alpha (ERα) pathway. This project will investigate how Tamoxifen affects the estrogenic activity of Minoxidil in estrogen receptor–positive breast cancer cells. Cells were maintained under hormone-deprived conditions and treated with estradiol, Tamoxifen, and a combination of Tamoxifen with Minoxidil. Cell proliferation was evaluated using the Alamar Blue assay to determine whether Tamoxifen reverses the proliferative effects of Minoxidil. A tryptophan emission assay will be performed to determine whether Minoxidil induces conformational changes in ERα; any fluorescence shift would indicate direct structural engagement with the receptor, supporting a mechanism of action involving ERα interaction As low-dose oral Minoxidil becomes widely prescribed to improve quality of life for patients coping with treatment-related hair loss, it is essential to ensure that its use does not compromise the effectiveness of hormone-directed therapy. The significance of this study lies in broadening our understanding of how Minoxidil operates at the molecular level. By examining its interaction with the estrogen receptor in estrogen receptor-positive breast cancer cells, we aim to uncover mechanisms beyond its known role as a potassium channel opener.