Repurposing Kir6/SUR2 Channel Activator Minoxidil to Arrest Growth of Gynecologic Cancers

May 2020 in “ Frontiers in pharmacology ”

Daniela F. Fukushiro-Lopes, Alexandra Hegel, Angela Russo, Vitalyi Senyuk, Margaret Liotta, Gyda Beeson, Craig C. Beeson, Joanna E. Burdette, Ronald K. Potkul, Sandro Gentile

minoxidil Kir6.2 SUR2 potassium channel activator reactive oxygen species ROS mitochondrial dysfunction DNA damage caspase-3 independent cell death pathway Rogaine

TLDR Minoxidil can stop the growth of ovarian cancer cells without harming the heart.

The study demonstrated that minoxidil, a Kir6.2/SUR2 potassium channel activator, could arrest the growth of gynecologic cancers, particularly ovarian cancer, by inducing cell death and reducing tumor growth in a xenograft model. Minoxidil's mechanism involved increasing reactive oxygen species (ROS) production, causing mitochondrial dysfunction, and leading to DNA damage, which activated a caspase-3 independent cell death pathway. The research found that high expression of the SUR2 gene was associated with improved survival in ovarian cancer patients. Minoxidil did not affect Kir6.2/SUR2 negative cells and did not produce cardiotoxic effects in mice, suggesting its potential as a safe and specific antiproliferative agent against ovarian cancer.

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