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Research Paper Volume 11, Issue 24 pp 12624—12640
Long noncoding RNA NNT-AS1 enhances the malignant phenotype of bladder cancer by acting as a competing endogenous RNA on microRNA-496 thereby increasing HMGB1 expression
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.