Fig. 7: EIF2AK3 knockdown enhanced DDP efficacy in vivo via autophagy inhibition. | Cell Death Discovery

Fig. 7: EIF2AK3 knockdown enhanced DDP efficacy in vivo via autophagy inhibition.

From: Hypoxia-triggered autophagy modulates cisplatin resistance in non-small cell lung Cancer via EIF2AK3-dependent PI3K/AKT signaling and mTOR-independent mechanisms

Fig. 7: EIF2AK3 knockdown enhanced DDP efficacy in vivo via autophagy inhibition.The alternative text for this image may have been generated using AI.

BALB/c nude mice were inoculated with A549 cells (5 × 106) stably transduced with sh-EIF2AK3, or sh-NC (n = 5 per group). Once the average tumor volume reached 50 mm³, mice were administered intraperitoneal injections of DDP (20 mg/kg daily for 7 days) and/or rapamycin (Rapa, 2 mg/kg every other day for 2 weeks), with PBS serving as the control. (A) Tumor volume was continuously monitored for 42 days. On day 42, the xenografts were removed (B) and weighed (C). D The protein expression of EIF2AK3 in xenograft tumor tissues was determined by immunohistochemistry assay. E The protein levels of EIF2AK3 cleaved caspase-3, LC3-II/I ratio, PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR in xenograft tumor tissues were measured. Data are presented as mean ± SD from three independent experiments (n = 5 per group). **p < 0.01, ***p < 0.001 versus sh-NC; #p < 0.05, ##p < 0.01, ###p < 0.001 versus sh-EIF2AK3.

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