Research Paper Volume 12, Issue 6 pp 5336—5351

Overexpressed ITGA2 contributes to paclitaxel resistance by ovarian cancer cells through the activation of the AKT/FoxO1 pathway

Figure 5. ITGA2 knockdown overcame drug-resistance induced by paclitaxel in ovarian cancers in vitro. (AD) SKOV3, OVCAR3, and A2780 cells lines were infected sh-Control or sh-ITGA2. Tumor cells were cultured at a density of 5x105 cells/well with or without the treatment of MK 2206 and with or without the treatment of PTX. After treatment for forty-eight hours, the tumor cells supernatants were collected to tested for levels of IL-6 (A) and IL-8 (B) and the tumor cells were harvested for caspase-Glo 3/7 assay (C) and western blot assay (D). Each bar represents the mean ± SD of three independent experiments. PTX treatment group was compared with no PTX treatment group. Statistical analyses were performed with one-way ANOVA followed by Tukey's multiple comparison's tests. ns, no significant; *, P < 0.05; ***, P < 0.001. (E) SKOV3, OVCAR3, and A2780 cells lines were infected sh-Control or sh-ITGA2. 48 hours post-infection, the cells were harvested for MTS assay with the treatment of PTX. Each bar represents the mean ± SD of five independent experiments. Each group was compared with sh-Control group. Statistical analyses were performed with one-way ANOVA followed by Tukey's multiple comparison's tests. **, P < 0.01; ***, P < 0.001.