Metapristone, the primary metabolite of RU486 (Axon 1502), suppressed NSCLC proliferation by promoting apoptosis via decrease the cellular EGFR-mediated PI3K/AKT pathways. In addition, metapristone inhibited anti-apoptotic marker Bcl-2, and activated pro-apoptotic key signaling proteins caspase-3, and poly (ADP-ribose) polymerase. Metapristone induced A549 and H1975 cell cycle via arrest at the G0-G1 stage. Moreover, metapristone inhibited endometrial cancer cell growth through suppressing cell proliferation and activating cell apoptosis-related signaling pathway. Mechanically, metapristone regulated miR-492 and its new target genes Klf5 and Nrf1 in vitro and in vivo to treat endometrial cancer.

KEYWORDS: Metapristone |Supplier | Metabolite Mifepristone | RU42633 | Desmethylmifepristone | RU 42633 | RU-42633 | CAS [104004-96-8] | Progesterone (PR) | Metabolite | Receptors