Skip to main content
Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: A novel long non-coding RNA lnc-GNAT1-1 is low expressed in colorectal cancer and acts as a tumor suppressor through regulating RKIP-NF-κB-Snail circuit

Fig. 3

Suppression of lnc-GNAT1-1 promoted proliferation, colony formation, cell motility, migration and invasion of SW480 cells. a The efficiency of lnc-GNAT1-1 knockdown was verified by real-time PCR, with the interference efficiency of around 90%. b Cell proliferation was determined by CCK8 assay, in which si-lnc-GNAT1-1 cells had a significant promoted proliferation rate than the control cells during a period of 96 h. c Plate colony formation assay showed increased colony formation ability of si-lnc-GNAT1-1 cells than the control cells (78.67 ± 4.51 vs. 157.30 ± 10.07, P < 0.001). d Cell cycle analysis showed that inhibition of lnc-GNAT1-1 could accelerate the cell cycle when compared with the control cells (G0/G1%: 45.50 ± 0.53% vs. 50.65 ± 0.31%, P < 0.001). e Flow cytometry analysis on apoptosis of cells showed that knockdown of lnc-GNAT1-1 decreased the number of apoptotic cells than control cells (10.17 ± 0.27%, 17.71 ± 0.26%, respectively, P < 0.001). f Wound healing assay during a period of 24 h showed an increased wound healing capacity of si-lnc-GNAT1-1 cells (Magnification × 100). g Transwell migration (upper) and invasion (lower) assays showed that enhanced migration (551.67 ± 21.83 vs. 208.67 ± 14.57, P < 0.001) and invasion (664.67 ± 31.70 vs. 246.00 ± 11.37, P < 0.001) capacities of SW480 cells following suppression of lnc-GNAT1-1 (Magnification × 100)

Back to article page