Fig. 5: FOXA1 prevented metabolic stress-induced autophagic cell death via activation of IGF2/IGF1R/mTORC1 signaling. | Cell Death & Disease

Fig. 5: FOXA1 prevented metabolic stress-induced autophagic cell death via activation of IGF2/IGF1R/mTORC1 signaling.

From: FOXA1 prevents nutrients deprivation induced autophagic cell death through inducing loss of imprinting of IGF2 in lung adenocarcinoma

Fig. 5: FOXA1 prevented metabolic stress-induced autophagic cell death via activation of IGF2/IGF1R/mTORC1 signaling.

A, B Status of the IGF1R/AKT/mTORC1 signaling pathway upon loss or gain of expression of FOXA in LUAD cells cultured in complete medium or PBS as evaluated by western blot assays. C Exogenous IGF2 expression levels in A549 cells as determined by RT-PCR or western blot assays. Mean ± SD, n = 3. D Survival of A549 cells with or without IGF2 forced expression as measured using colony formation assays. Mean ± SD, n = 3. E Survival of PC-9 cells in nutrients deprived conditions upon treatment with linsitinib (0.5 μM), anti-IGF2 antibodies (0.5 μg/mL), anti-VEGF antibodies (0.5 μg/mL), or rapamycin (50 nM) were determined using colony formation assays. Mean ± SD, n = 3. F Colony formation assays demonstrated that supplementation with recombinant IGF2 restored survival in FOXA1-deficient PC-9 cells under metabolic stress conditions. Mean ± SD, n = 3. G Colony formation assays demonstrated that stable expression of IGF2 restored survival in FOXA1-deficient PC-9 cells under metabolic stress conditions. Mean ± SD, n = 3. H Colony formation assays indicated that treatment with IGF2 antibody (0.5 μg/mL), VEGF antibody (0.5 μg/mL), linsitinib (0.5 μM) or rapamycin (50 nM) abolished the protective effects of FOXA1 expression on A549 cells in nutrients deprived conditions. Mean ± SD, n = 3. *P < 0.05; **P < 0.01; ***P < 0.001, NS not significant.

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