The effects of rapamycin on the glycolysis in breast cancer cell lines MCF-7 & MDAMB231

Introduction: Cancer cell supply energy mainly through glycolysis. Akt is one of the master regulator increase the flow rate of glycolysis. in addition, activation and stimulation of mTOR1 is another important function of Akt. mTOR1 also play a key role in energy and macromolecules production for cancer cell. Rapamaycin is a drug that inhibits mTOR1 function, but activates Akt signal pathway through negative feedback. Recently, rapamaycin is approved for cancer treatment, but its effectiveness is not complatly satisfactory. Activation of glycolysis maybe the main hypothesis for ineffectiveness of rapamycin. The current study was conducted to investigate the effect of rapamycin on glycolysis. Methods: In this study, after culturing cancer cells and adding drug rapamycin to cells, The activity of the enzyme lactate dehydrogenase as the main marker of glycolysis pathway was determined. Results: The growth of MCF-7 Cells was inhibited by Rapamaycin but The growth of MDA-MB231 Cells was not inhibited. LDH activity was increased in MDAMB231 Versus the control group, but LDH activity redused in MCF-7 Cells. Discussions: Activation of glycolysis pathway by Rapamaycin was detected in MDAMB231 Cells but not in MCF-7 Cells. Increasing of glycolysis as the main stream of energy production by Rapamaycin in MDA-MB231 Cells be considered a reason for effectiveness of this drug on MDA-MB231 Cells. MDA-MB231 is a malignant Cells with highly the flow glycolysis. The underlying mechanism for LDH activation by Rapamaycin should be consider for Future studies.

کلیدواژه ها:

Rapamycin ، Glycolysis ، MCF-7 & MDAMB231