Research Paper Volume 13, Issue 5 pp 6804—6819

Transcription factor ELK1 accelerates aerobic glycolysis to enhance osteosarcoma chemoresistance through miR-134/PTBP1 signaling cascade

ELK1 facilitates chemoresistance of osteosarcoma cells to DXR by increasing enhancing aerobic glycolysis through miR-134/PTBP1 axis. DXR-resistant cells (U2OS/DXR) were treated with expression vector containing PTBP1 gene or siRNA targeting ELK1 gene and/or exogenous miR-134 mimic or miR-134 inhibitor. (A) The consumption of glucose and lactic acid and the ratio of ATP production in U2OS/DXR cells. (B) Protein levels of GLUT3, HK2, and PDK1 in U2OS/DXR cells. (C) IC50 in U2OS/DXR cells detected using CCK8 assay. (D) Cell viability in U2OS/DXR cells detected using EdU assay. Values obtained from three independent experiments in triplicate are analyzed by unpaired t test. *p

Figure 7. ELK1 facilitates chemoresistance of osteosarcoma cells to DXR by increasing enhancing aerobic glycolysis through miR-134/PTBP1 axis. DXR-resistant cells (U2OS/DXR) were treated with expression vector containing PTBP1 gene or siRNA targeting ELK1 gene and/or exogenous miR-134 mimic or miR-134 inhibitor. (A) The consumption of glucose and lactic acid and the ratio of ATP production in U2OS/DXR cells. (B) Protein levels of GLUT3, HK2, and PDK1 in U2OS/DXR cells. (C) IC50 in U2OS/DXR cells detected using CCK8 assay. (D) Cell viability in U2OS/DXR cells detected using EdU assay. Values obtained from three independent experiments in triplicate are analyzed by unpaired t test. *p < 0.05 compared with U2OS/DXR cells treated with si-NC; # p < 0.05 compared with U2OS/DXR cells treated with oe-NC; ! p < 0.05 compared with U2OS/DXR cells treated with mimic NC; & p < 0.05 compared with U2OS/DXR cells treated with inhibitor NC; @ p < 0.05 compared with U2OS/DXR cells treated with si-ELK1 + inhibitor NC; % compared with U2OS/DXR cells treated with miR-134 mimic + oe-NC.