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. 2015 Jul 16;5:12230. doi: 10.1038/srep12230

Figure 3. The up-regulation of A3G induces anoikis resistance.

Figure 3

(A,B) The establishment of stable A3G knockdown BxPC3 cells. BxPC3 cells with stable A3G knockdown were established by recombinant lentiviral infection. Real-time qPCR and western blots revealed that A3G levels were significantly lower in stable A3G knockdown BxPC3 cells than in controls (**P < 0.01, Student’s t-test). (C) A3G expression increases the colony formation rate. Representative images from the colony formation assay for stable A3G-expressing BxPC3 cells and A3G knockdown BxPC3 cells are shown in the upper panels. The colony formation rate of A3G-overexpressing cells was significantly higher than control cells, while the colony formation rate of A3G knockdown cells was significantly lower than control cells. All data are represented as the means ± SEM of triplicate experiments (*P < 0.05, **P < 0.01, ANOVA) (Scale bar 100 μm). (D) Determination of Caspase 3/7 activities. Caspase 3/7 activities were inhibited in stable A3G-expressing cells after detachment (*P < 0.05, Student’s t-test). (E) A3G induces anoikis resistance. Stable A3G-expressing BxPC3 cells and A3G knockdown BxPC3 cells were stained with Annexin V/APC in attached and detached states and were subjected to flow cytometry analyses. In the detached state, stable A3G-expressing cells showed suppressed anoikis (upper 4 panels); meanwhile, stable A3G knockdown cells showed the promotion of anoikis after detachment (lower 4 panels).