Fig. 4: Combination treatment of Icotinib and AT101 dramatically inhibited TKI-resistant tumor growth in a xenograft model. | Cell Death & Disease

Fig. 4: Combination treatment of Icotinib and AT101 dramatically inhibited TKI-resistant tumor growth in a xenograft model.

From: APE1 stimulates EGFR-TKI resistance by activating Akt signaling through a redox-dependent mechanism in lung adenocarcinoma

Fig. 4: Combination treatment of Icotinib and AT101 dramatically inhibited TKI-resistant tumor growth in a xenograft model.

a Tumor growth curve. Xenograft models are generated by HCC827/IR cells. When tumor volume reached approximately 100 mm3, mice were treated with Icotinib (4 mg/kg, IP) or AT101 (35 mg/kg, oral injection) or combination for 10 days. Mice were killed 10 days after drug treatment. Asterisk indicates compared to control group; hash indicates compared to combination treatment group. ***p < 0.001; ###p < 0.001. b Tumor weight. At the end of the animal experiment, tumors were collected from mice and weighed. c Combination of AT101 and Icotinib significantly inhibited cancer cell proliferation. Ki-67 expression was detected by immunohistochemistry. d Combination of AT101 and Icotinib significantly increased and inhibited pro- and anti-apoptotic protein expression, respectively

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