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. 2019 Aug 10;47:195–207. doi: 10.1016/j.ebiom.2019.07.068

Fig. 6.

Fig. 6

ITGA6 promoted the growth and progression of bladder cancer cells in vitro and in vivo.

a–c Effects of forced expression of ITGA6 on the adhesion (a), proliferation (b), and migration (c) of SV-HUC-1 cells. Bar = 100 μm, 200×. d–g Effects of ITGA6 knockout on the adhesion (d), proliferation (e), migration (f), and invasion (g) of 5637 cells. Bar = 100 μm, 200×. h Sphere formation assay to determine the SFE in control and ITGA6-depleted (KO-ITGA6) 5637 cells. Bar = 50 μm, 50× and 200×. i Subcutaneous tumour model of KO-ITGA6 T24 cells. Tumour images, growth curves, and weights at the endpoint are shown. j In vivo tumour metastasis model of KO-ITGA6 T24 cells. The graph represents the number of lung nodules. Formation of T24 cell metastatic foci in the lung was confirmed by H&E staining. Bar = 200 μm, 100×. k–n Effects of forced expression of ITGA6 in KO-METTL3 T24 cells. ITGA6 partially restored the cell adhesion (k), proliferation (l), migration (m), and invasion (n) capacities in T24 cells, which were reduced by METTL3 knockout. o The schematic model of the role and underlying mechanism of m6A-mediated ITGA6 in bladder cancer development. All bar plot data are the means ± SDs or means ± SEMs of three independent biological replicates. *p < .05, **p < .01, ***p < .001, ****p < .0001. (Student's t-test, one-way ANOVA, Tukey's multiple comparisons test).