Metapristone (RU486-derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis

Abstract Background Endometrial cancer is an invasive gynecological prevalent in the world. The pathogenesis of endometrial related to multiple levels regulation, referring oestrogen, tumor-suppressor gene (e.g. PTEN ) or microRNAs miR-23a and miR-29b). Metapristone a hormone-related drug, which widely used clinical treatment cancer. However, underlying regulatory mechanism metapristone on still unclear, especially effect microRNAs. aim this study investigate specific molecular regulating Methods RL95-2 cells Ishikawa were as models. MiR-492 si-miR-492 was transfected into explore role miR-492 cell model mice confirm function affected vitro vivo. Mechanically, proliferation monitored using MTT assay, colony formation assay EdU assay. Luciferase reporter identify downstream target miR-492. protein expression RNA respectively measured by western blot qRT-PCR for signaling pathway research, subsequently, verified tumor via immunohistochemistry. Results kind drug significantly inhibited growth through apoptosis-related expression. its genes Klf5 Nrf1 highly expressed lines, promoted apoptosis. decreased , leading inhibition Conclusion decreasing ( ), provided theoretical basis