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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Targeting of the AXL receptor tyrosine kinase by small molecule inhibitor leads to AXL cell surface accumulation by impairing the ubiquitin-dependent receptor degradation

Fig. 3

GAS6 mRNA levels were significantly different in Hs578T, H292 and H1792 cells. H1792 cells showed significant induction by serum deprivation. a H292 exhibited a 429-fold expression of GAS6 mRNA and Hs578T a 96-fold higher expression compared to H1792 cells. RT-qPCR demonstrated no different expression of GAS6 mRNA in Hs578T, H292 and H1792 cells after medium exchange for 2 hours and 6 hours with serum containing culture medium (+FCS) or serum depleted medium (−FCS). b GAS6 mRNA was significantly induced by serum deprivation in H1792 cells after 12 and 24 h of serum depletion. GAPDH and ALAS served as normalization controls utilizing the ΔCT method for (A) and the ΔΔCT method for (B). c, e, g Treatment with exogenous GAS6 led to AXL degradation in Hs578T and H1792 cells. BMS777607 (BMS) prohibited lysosomal degradation more efficiently than QC. AXL abundance in Hs578T, H292 and H1792 cells after treatment with AXL TKI BMS or the lysosomal acidification inhibitor Chloroquine (CQ) for 3 hours in combination with 250 ng/ml of recombinant GAS6 for 2 hours is shown. ACTIN served as normalization control. Mean values and SEM of three (H1792), four (H292) and five (Hs578T) independent experiments are shown. d, f, g Representative western blots are displayed for Hs578T, H292 and H1792 cells. Differences with *P < .05, **P < .01, and ***P < .001 were considered statistically significant

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