Fig. 5

Metapristone inhibited the tumor growth through regulating miR-492 and its downstream target genes Klf5 and Nrf1 in vivo. a The tumor xenograft model of RL95-2 cells and Ishikawa cells. (n = 6 per group). b The expression of Ki-67 and Cleaved-caspase 3 in the tumor xenograft of RL95-2 cells and Ishikawa cells with or without metapristone treatment were detected by immunohistochemistry. Magnification: × 200. c The expression of Klf5 and Nrf1 in the tumor xenograft of RL95-2 cells and Ishikawa cells with or without metapristone treatment were detected by immunohistochemistry. Magnification: × 50. d The mRNA expression of miR-492, Klf5 and Nrf1 in the tumor xenograft of RL95-2 cells and Ishikawa cells with or without metapristone treatment were measured by real-time PCR (n = 6 per group). Values are means ± SD. e The protein expression of Klf5 and Nrf1 in the tumor xenograft of RL95-2 cells and Ishikawa cells with or without metapristone treatment were measured by western blot (n = 6 per group). Values are means ± SD. f The schematic representation of metapristone inhibitory effect on endometrial cancer cells through regulating cell proliferation and apoptosis and miR-492/Klf5/Nrf1 axis