Skip to main content
. Author manuscript; available in PMC: 2018 Apr 19.
Published in final edited form as: Cancer Res. 2012 Nov 1;73(1):331–340. doi: 10.1158/0008-5472.CAN-12-3151

Figure 2. AXL promotes survival of esophageal adenocarcinoma cells.

Figure 2

A) Cell viability of OE33 cells stably expressing AXL or empty vector in response to CDDP was assessed by CellTiter-Glo Luminescent Cell Viability Assay. Western blot analysis of AXL in OE33/AXL and OE33/pcDNA4 stable cells is shown (upper panel). Cell survival of AXL-expressing cells was significantly higher than control cells in response to CDDP (lower panel). B) Cell viability of FLO-1 cells stably expressing AXL shRNA or control shRNA in response to CDDP was determined as in panel A. Immunoblot of AXL is shown (upper panel). Knockdown of AXL in FLO-1 cells significantly decreased cell viability in response to CDDP (lower panel). C) OE33 cells stably expressing AXL or pcDNA4 were subjected to clonogenic survival assay after treatment with vehicle or CDDP (2.5 μmol/L) for 48h. Quantitative data (right panel) showed significantly higher cell survival in AXL-expressing cells than control cells (p<0.01). D) FLO-1 cells stably expressing AXL shRNA or control shRNA were treated with CDDP (5 μmol/L) for 48h, and subjected to clonogenic survival assay. Quantitative data (right panel) indicated that knockdown of endogenous AXL significantly decreased cell survival relative to control in response to CDDP (p=0.01). Results are representative of at least three experiments and shown as the mean ± SD. *p<0.05, ***p<0.001.