Fig. 3

TESC serves as a target of ROR. a Real-time PCR measurement of mRNA expression of TESC. The expression levels of TESC in tumor cells were significantly higher than normal. Once ROR was silenced in tumor cells, there was a remarkable decrease in TESC expression. NCM460: normal colon cell; GES-1: normal gastric cell. b Overlapping altered genes from lncRNA-ROR knockdown cells from AGS and HT29 cells. By using four-fold changes as baseline, there were approximately 58 altered genes after depletion of ROR in AGS and 125 altered genes in HT29. A total of six genes were changed in AGS and HT29 cells after ROR knockdown. c Western blot showing that the expression of TESC in ROR silenced AGS and HT29 tumor cells. The expression of TESC was greatly decreased in ROR-depleted tumor cells as well as in normal cells, including fibroblasts, normal colon cell NCM460, and normal gastric cell GES-1. d, e Silenced expression of TESC using siRNAs in AGS (d) and HT29 cells (e). Real-time PCR demonstrated siTESC provided the optimal deletion of TESC. Experiments were performed 48 h following siTESC (125 pmol) and control siRNA(125 pmol) treatment. *P <0.05: compared with the control and NC. NC: non-silencing control. f Western blot demonstrating that siTESC efficiently silenced TESC at the protein expression level in AGS and HT29 cells. All experiments were performed 48 h following siTESC (125 pmol) and control siRNA (125 pmol) treatment. NC: non-silencing control. g RT-PCR showing that ROR expression was not significantly changed when TESC was silenced in AGS and HT29 cells