LAUSR

Simple Summary This review informs on how the MYC signaling is dysregulated and participates in ovarian cancer progression, and the unmet challenge to directly target MYC for ovarian cancer treatment. Therefore, we proposed to alternatively target essential downstream polyamine metabolism pathway of MYC. In this review we include the metabolism of polyamine, the regulation of polyamine metabolism by MYC signaling, the utility of polyamine as therapeutic targets and cancer biomarkers. Abstract c-MYC and its paralogues MYCN and MYCL are among the most frequently amplified and/or overexpressed oncoproteins in ovarian cancer. c-MYC plays a key role in promoting ovarian cancer initiation and progression. The polyamine pathway is a bona fide target of c-MYC signaling, and polyamine metabolism is strongly intertwined with ovarian malignancy. Targeting of the polyamine pathway via small molecule inhibitors has garnered considerable attention as a therapeutic strategy for ovarian cancer. Herein, we discuss the involvement of c-MYC signaling and that of its paralogues in promoting ovarian cancer tumorigenesis. We highlight the potential of targeting c-MYC-driven polyamine metabolism for the treatment of ovarian cancers and the utility of polyamine signatures in biofluids for early detection applications.