Skip to main content
. 2019 Dec 17;11(24):12624–12640. doi: 10.18632/aging.102591

Figure 6.

Figure 6

The oncogenic functions of NNT-AS1 in bladder cancer cells are mediated by stimulation of the miR-496–HMGB1 axis output. (A) T24 and TCC-SUP cells were transfected with either the miR-496 inhibitor or NC inhibitor. After 48 h, the transfection efficiency was assessed by RT-qPCR. *P < 0.05 vs. NC inhibitor. (B, C) siNNT-AS1 plus either the miR-496 inhibitor or NC inhibitor were cotransfected into T24 and TCC-SUP cells. The miR-496 and HMGB1 protein levels were measured by RT-qPCR and western blotting, respectively. *P < 0.05 vs. group siNC. #P < 0.05 vs. group siNNT-AS1+NC inhibitor. (D–G) CCK-8 assay, flow-cytometric analysis, and transwell migration and invasion assays were performed to determine the status of proliferation, apoptosis, migration, and invasiveness of T24 and TCC-SUP cells that were cotransfected with siNNT-AS1 and either the miR-496 inhibitor or NC inhibitor. *P < 0.05 vs. the siNC group. #P < 0.05 vs. group siNNT-AS1+NC inhibitor.