Fig. 5

LINC00240 represses DDX21 degradation via the ubiquitin–proteasome pathway. A, B Western blot analyses of DDX21 protein in cells with stable knock-down of LINC00240 or enforced expression of LINC00240. C, D Treatment of the stably LINC00240-knock-down gastric cancer cells with the 26S protostome inhibitor MG132 elevated expression of DDX21 protein. E, F Treatment of gastric cancer cells with MG132 eliminated LINC00240-induced upregulation of DDX21 protein expression. G, H Gastric cancer cells with stable LINC00240-knockdown, overexpression of LINC00240 and control cells were treated with cycloheximide (CHX) for the indicated periods of time. I Western blot of the ubiquitination of DDX21 in cells that stabilized silenced LINC00240 or over-expressed LINC00240. J Silencing of DDX21 with siRNAs significantly inhibited proliferation of HGC-27 or MGC80-3 cells with stably overexpressed LINC00240. J Over-expression of DDX21 could enhance growth of gastric cancer cells with stable silencing of LINC00240 with shRNAs. Data are shown as mean ± SD. ***P < 0.001 by unpaired Student’s t test (J, K). ns: not significant