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. 2016 Mar 8;7(15):20561–20573. doi: 10.18632/oncotarget.7987

Figure 3. Overexpression of RalA in K562 cells confers IM resistance.

Figure 3

(A) K562 cells transfected with RalA plasmid, empty vector or blank were treated with different concentrations of imatinib (0–0.15 μM) for 48 h, followed by MTT assays. (B) Overexpression of RalA reduces apoptosis following IM treatment. K562 cells transfected with RalA plasmid, empty vector or blank were treated with IM (0.1 μΜ) for 48 h. The cells were washed and stained with 7-AAD and then analyzed by flow cytometry to determine apoptosis. Statistical significance was assessed by one-way ANOVA (*p < 0.05). (C) Colony formation assays. A total of 1000 cells transfected without or with control or RalA plasmids were mixed with RPMI-1640 medium containing 0.9% methylcellulose solution, 20% FBS and IM (0.75 μΜ), and seeded onto 24-well plates. Colony numbers were counted after 1 week. (D). Xenograft model of CML with the human cell line K562 with RalA or empty vector in Balb/c mice. 500,000 K562 cells transfected with RalA or empty vector were injected via intravenous tail vein injection into sublethally irradiated (3 Gy) Balb/c recipient mice. Imatinib was injected intraperitoneally at a dose of 100 mg/kg body weight for 10 consecutive days. Overall survival is shown by Kaplan–Meier analysis.