Fig. 2: CRABP2 promoted the oxaliplatin resistance of GC cells. | Cell Death & Disease

Fig. 2: CRABP2 promoted the oxaliplatin resistance of GC cells.

From: Upregulation of CRABP2 by TET1-mediated DNA hydroxymethylation attenuates mitochondrial apoptosis and promotes oxaliplatin resistance in gastric cancer

Fig. 2

a After knocking down CRABP2, the viability of AGS-OXA and HGC-27-OXA cells was determined under different concentrations of OXA. b After knocking down CRABP2, the colony forming ability of AGS-OXA and HGC-27-OXA cells was determined in the absence or presence of OXA (concentration: 2.0 μM). c The cell apoptosis results of AGS-OXA and HGC-27-OXA cells after knocking down CRABP2 in the presence or absence of OXA (concentration: 2.0 μM) by flow cytometry. d In the presence of different concentrations of OXA, AGS and HGC-27 cells overexpressing CRABP2 were determined by cell viability assay. e In the presence or absence of OXA (concentration: AGS 0.2 μM, HGC-27 0.4 μM), AGS and HGC-27 cells overexpressing CRABP2 were determined by the colony forming assay. f In the absence or presence of OXA (concentration: AGS 0.2 μM, HGC-27 0.4 μM), the cell apoptosis results of AGS and HGC-27 cells overexpressing CRABP2 were determined by flow cytometry. All experiments were performed in three replicates. The data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

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