Glucose metabolism of lung adenocarcinoma A549 cells and its correlation with taxol-resistance
10.3781/j.issn.1000-7431.2013.04.001
- Author:
Shi-Yan ZHAO
1
Author Information
1. Department of Nuclear Medicine
- Publication Type:Journal Article
- Keywords:
Dichloroacetate;
Glucose;
Lipid;
Lung neoplasms;
Metabolism;
Paclitaxel
- From:
Tumor
2013;33(4):299-303
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the difference in glucose metabolism between lung adenocarcinoma A549 cell line and its taxol-resistant (A549/taxol) cell line, and to determine the effect of DCA (dichloroacetate) on glucose metabolism of these two cell lines. Methods: The taxol resistance of A549 and A549/taxol cell lines were firstly determined by CCK-8 (cell counting kit-8) assay. Then the productions of CO2 and lipid in A549 and A549/taxol cells were detected by scintillation counter after treatment with 14C-glucose. Furthermore, the uptake of 18F-FDG (18F-2-deoxy-β-D- glucose) and the production of lactate were detected by y-counter and lactate measurement kit, respectively. Results: All of CO2 production level, the 18F-FDG uptake rate and the lactate production level after treatment with 6-14C-glucose were lower in A549/taxol cells than those in A549 cells. The level of CO2 production after treatment with 6-14C-glucose was significantly higher in A549 cells treated with DCA than that in A549 cells without DCA treatment. However, DCA had no effect on the CO2 production after treatment with 6-14C-glucose in A549/taxol cells. Conclusion: There is a certain extent of mitochondrial oxidative breathing suppression in A549/taxol cells. DCA can promote mitochondrial oxidative respiration in A549 cells, but has no effect on that in A549/taxol cells. Copyright © 2013 by TUMOR.
