75 69.02 ± 2.98   M3:15.71 ± 0.78 15.84 ± 0.81 15.93 ± 0.84   M4:25.98 ± 1.24 24.18 ± 1.16 9.48 ± 0.56 M1: the percentage of apoptotic cells, M2: G0/G1 stage cells, M3: S stage cells, M4: G2/M stage cells. In the End1/E6E7 cells,

there was no significant difference existed in cell cycle among the cells without transfection, transfected with control plasmid and transfected with siRNA. In the HeLa cells, after transfection with siRNA TKTL1, the percentage https://www.selleckchem.com/products/z-vad-fmk.html of G0/G1 stage cells was increased, the percentage of G2/M stage cells was significantly reduced. The effect of siRNA TKTL1 on cell proliferation in HeLa and End1/E6E7 cell line To examine the effect of siRNA TKTL1 on cell proliferation, the absorption values of one culture plate from each group cells were detected by using MTT at 490 nm on daily basis for a period of five days. The growth curve of each cell group showed that cell proliferation was slower in the HeLa cells transfected siRNA TKTL1 construct than the cells transfected with control plasmid, or cells without transfection (Fig 3). There was no

significant difference of cell proliferation among the End1/E6E7 cells without transfection, transfected with control plasmid and transfected with siRNA. Those results suggested that cells proliferation was inhibited by transfected siRNA TKTL1 construct in the HeLa cells. While, there was no significant difference on cell proliferation in normal cells after transfected siRNA TKTL1 construct. Figure 3 The effect of anti-TKTL1 siRNA on proliferation of End1/E6E7 cells and HeLa cells. In the End1/E6E7 cells (A), There was no significant MCC950 solubility dmso difference of cell proliferation among the cells without transfection, transfected with control plasmid and transfected with siRNA. In the HeLa cells (B), cell proliferation was significantly inhibited after transfected siRNA TKTL1 construct. Discussion Tumor cells need VAV2 a large amount of energy and nucleic acids

to survive and grow. For most of their energy needs, malignant cells typically depend on glycolysis mainly, the anaerobic breakdown of glucose into ATP [1]. Malignant cells characteristically exhibit an increased reliance on anaerobic metabolism of glucose to lactic acid even in the presence of abundant oxygen had been described by Warburg 80 years ago [2]. But, this theory was gradually discredited. Latter Following the development of bioenergetics, recent studies demonstrated that energy metabolism in malignant cells is significantly enhanced compared to those in the normal cells, especially glycometabolism [1]. The malignant cells maintain ATP production by increasing glucose flux because anaerobic metabolism of glucose to lactic acid is substantially less efficient than KPT-8602 oxidation to CO2 and H2O. PET imaging has demonstrated a direct correlation between tumor aggressiveness and the rate of glucose consumption [10, 11].