Fig. 8

Knockdown of NR3C1 inhibits the proliferation and migration of ccRCC by activating ATF6. A Schematic overview for B–K. B Inhibition of ATF6 rescued the NR3C1 knockdown-mediated reduced colony formation ability of ACHN and 786-O cells, as assessed using clone formation assays. (Scale bar =100 μm). C Bar graphs represent the colony formation results in ACHN and 786-O cells. Inhibition of ATF6 rescued the NR3C1 knockdown-mediated altered proliferative capacity of ACHN (D) and 786-O (E) cells, as assessed using EdU assays. (Scale bar =100 μm). F Bar graphs represent the EdU results in ACHN and 786-O cells. Inhibition of ATF6 rescued the NR3C1 knockdown-mediated altered migration ability of ACHN (G) and 786-O (H) cells, as assessed using wound healing assays. Images were acquired at 0, 8 and 16h. (Scale bar =700 μm). I Inhibition of ATF6 rescued the NR3C1 knockdown-mediated reduced migration ability of ACHN and 786-O cells, as assessed using Transwell assays. Images were acquired at 12h. (Scale bar =100 μm). J Bar graphs show the scratch healing area in ACHN and 786-O cells at 8 and 16h. K Bar graphs represent the results of Transwell assays in ACHN and 786-O cells. The cells in the rescue group were pretreated with 20 µM ATF6i for 24h. Data presented as mean  ±  SD with three replicates. Ns, no significant difference; *P <  0.05; **P <  0.01; ***P <  0.001; ****P <  0.0001. ATF6i, Ceapin-A7 as ATF6 inhibitor