Fig. 3: The neutralization effect of IGF2R on IGF1R signaling is negligible in cervical cancer. | Cell Death & Disease

Fig. 3: The neutralization effect of IGF2R on IGF1R signaling is negligible in cervical cancer.

From: Upregulation of IGF2R evades lysosomal dysfunction-induced apoptosis of cervical cancer cells via transport of cathepsins

Fig. 3

a Co-localization of IGF2R (green) and IGF-2 (red) in cervical cancer cells. b Influence of IGF2R on IGF-2 degradation. At 96 h after IGF2R knockdown, cells were stained with anti-IGF-2 (green) and anti-LAMP1 (red) antibodies. c Activation of IGF1R signaling pathways in cervical cancer cells. The phosphorylation of IGF1R and its downstream kinases were analyzed by western blot analysis. In addition to IGF2R knockdown samples at 24 h after siRNA transfection, other samples that recovered at 15 min after stimulation by their ligands (IGF-1 and IGF-2) were also analyzed. d Combined effect of IGF2R and IGF1R knockdown on cell viability. The knockdown of each receptor was confirmed by western blot analysis (top panel). The bottom panel shows the viability of cells at 144 h after transfection e Phosphorylation profile of major RTKs signaling in IGF2R-knockdown cells at 72 h after siRNA transfection. A complete target map is shown in the bottom panel. f Time-dependent changes in p38 MAPK phosphorylation status after IGF2R knockdown. h Rescue effect of p38 MAPK inhibition on IGF2R knockdown-induced cell death. siRNA-transfected cells were further exposed to 1 μM SB203580 (p38 MAPK inhibitor) for 96 h, and their viabilities were measured. All the error bars represent the standard deviation of three independent experiments. *p < 0.05, **p < 0.01, ****p < 0.0001; Dunnett’s multiple comparisons test. Scale bars represent 20 μm.

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