| Part1: The effects of DCA on the “aerobic glycolysis”, the cellviability and the apoptosis of the cell linesOBJECTIVE: To investigate the effects of DCA on the “aerobicglycolysis”, the cell viability and the apoptosis of the cell lines.METHODS: we detected the ability of the glucose uptaken, lactateproduction and the ROS level in the DCA-treated cells and thecontrol cells; we also investigated the difference of the cell viabilityand the apoptosis rate between the DCA-treated cells and controlcelsl. RESULTS: DCA can significantly inhibit the glucose uptakenand the lactate production, and increase the ROS level as well inthe cancer cells, while sparing normal cells Lo2. DCA aslo inhibitthe cell viability and induce the apoptosis of the cancer cell linesSGC-7901and HCC-LM3, while sparing normal cells Lo2. Theseaffects on the cancer cells by DCA were reversed by the ROSscavenger NAC. And DCA also increase the expression of PUMAprotein in the two cancer cell lines. CONCLUSION: DCA can specificly regulate the glucose metabolism in cancer cells, whilesparing normal cells. The increased ROS level according to theupregulated Oxidative Phosphorylation can inhibit the cellviability and induce the apoptosis in cancer cells. Part2: DCA inhibit the invasive ability of the SGC-7901andHCC-LM3cell line in vitro.OBJECTIVE: To investigate the effects of DCA on invasive abilityof human gastric cancer cell line SGC-7901and hepatic cancer cellline HCC-LM3in vitro. METHODS: Measuring the difference ofpHe between the DCA treated cancer cells and the control cells;evaluating the invasive ability of cancer cells by the transwell testcoated with the matrigel, wound healing test and the adhensiongassay. Examing the expression of the MMP-2and MMP-9in cancercells treated or not by DCA. RESULTS: DCA can inhibit theinvasion ability of cancer cells; and did not affect cancer celladhesion and migration. Taken together, our data suggest thatDCA can specifically inhibit the degradation of matrigel (asurrogate of ECM); the expression of MMP-2and MMP-9inDCA-treated SGC-7901cells was much lower than control cells.CONCLUSION: Our data suggest that DCA can specificallyinhibit the matrix remodeling by neutralizing the acidicmicroenvironment. Part3: DCA inhibits the metastasis of SGC-7901-luc cells invivo and prolong the survival time of xenograftsOBJECTIVE: To explore the effects of DCA on malignantbiological behavior of human gastric cancer orthotipictransplantation nude mice model in vivo. METHODS: The humangastric cancer cell line SGC-7901-luc was selected for this research.Construct the human gastric cancer orthotopic transplantationnude mice model. Use in vivo bioluminescence imagingtechnology to monitor the invasion ability of human gastric cancerin vivo. RESULTS: The sumgrey and the lesion area betweenDCA-treated group and control group is similar at base line, butwere significantly lower in DCA-treated group than in the controlgroup. DCA significantly prolonged the survival time of micebearing SGC-7901-luc cells (p=0.002) CONCLUSION: DCA caninhibit the invasion of SGC-7901-luc cells in vivo and prolong thesurvival time of xenografts bearing SGC-7901-luc cells. |
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