Fig. 2.
DHX9 promotes the proliferation of colorectal cancer cells in vitro. A CRC cells with untreated (Control), lentiviral vector-transfected (pLVX), stably expressing DHX9-encoding constructs (pLVX-DHX9) or shRNAs against DHX9 (pLVX-shDHX9) were subjected to DHX9 expression analysis by RT-qPCR assay. ns, not significant; ***P < 0.001. B Western blotting assay to analyze DHX9 transfection efficiency in CRC cells. Left, the representative ECL images detected by Western blotting analysis. Right, the summary data in CRC cells correspond to Left (n = 3). ns, not significant; *P < 0.05; **, P < 0.01; ***, P < 0.001. C OD490nm values of CRC cells with untreated, vector-transfected, stably expressing DHX9-encoding constructs or shRNAs against DHX9 for indicated time. ns, not significant; ***P < 0.001. D DHX9-overexpressed and -silenced CRC cells were subjected to trypan blue exclusion assay. ***P < 0.001. E The mRNA levels of MKI67 encoding Ki67 in CRC cells with untreated, vector-transfected, stably expressing DHX9-encoding constructs or shRNAs against DHX9 were detected by RT-qPCR analysis. F Anchorage-independent colony growth of CRC cells with untreated, vector-transfected, stably expressing DHX9-encoding constructs or shRNAs against DHX9 were determined. ns, not significant; ***P < 0.001. All data in bar graphs were shown as mean ± SEM from three independent experiments and assessed by one-way ANOVA, post hoc intergroup comparisons, Tukey’s test