Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancer.

ABSTRACT: Atovaquone, an FDA-approved oxidative phosphorylation (OXPHOS) inhibitor, has shown promise in the treatment of epithelial ovarian cancer (EOC), the deadliest gynecologic malignancy. However, the precise mechanisms underlying its antitumorigenic effects remain unclear. We employed a longitudinal transcriptomic approach to characterize the molecular effects of atovaquone on EOC cells. Our findings demonstrate that atovaquone disrupts cellular homeostasis and metabolism, activates stress responses, and primes immune recognition. We observed temporal downregulation of genes and pathways involved in key cellular processes, such as the cell cycle and DNA replication, which correlated with reduced proliferative capacity. Atovaquone also downregulated both OXPHOS and glycolysis while upregulating

SUBMITTER: Betancourt Ponce M 

PROVIDER: S-EPMC12644797 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature