Fig. 8

Oxamate abrogates LDLc or HDLc promoted proliferation of colon cancer cells. A-D Crystal violet staining for quantification of cell survival/proliferation. HCT-116 and HCT-15 cells were treated with oxamate (15 mM) in the presence or absence of LDLc/HDLc (50 μg/ml) for 48 h, and crystal violet staining was performed. A, B HCT-116 treated with oxamate in the presence or absence of LDLc and HDLc respectively. C,D HCT-15 cells treated with oxamate in the presence or absence of LDLc or HDLc respectively. Bar graphs represent the relative intensity indicative of % survival. Experiments were done in triplicate. E Targeting the glycolytic function of colon cancer cells with oxamate treatment in the presence or absence of LDLc or HDLc. HCT-116 cells were pre-treated with vehicle or 50 μg/ml of LDLc/HDLc with or without oxamate for 12 h in 1% FBS-containing media, followed by the analysis of various glycolytic parameters in the presence of vehicle or 50 μg/ml LDLc/HDLc through XeF24 seahorse analyzer. The graph represents the glycolytic stress (ECAR) functional analysis. The experiment was done in triplicate