Metabolic reprogramming has been shown in many cases to be essential for tumorigenesis. The Mitochondrial Pyruvate Carrier (MPC) plays a key role in this metabolic switch since it couples glycolysis and mitochondrial oxidation. The MPC is a hetero-complex formed by two subunits, MPC1 and MPC2. While MPC1 is found within the most frequently deleted region across all cancers, MPC2 expression is more variable. Here we used lung cancer A549 cells as model, where MPC1 is downregulated while MPC2 is well expressed. We generated A549 cells in which MPC expression was either depleted or increased. Mitochondrial respiration in a cell culture assay showed that the MPC2 knock-down cell line showed lower respiration rates compared to A549 wild-type (WT), while MPC1 overexpression reduced cell proliferation. As part of this project, we attempted to monitor pyruvate transport using two fluorescent probes, PyronicSF and MitoPyronicSF, however in our hands these probes did not function as expected and we were unable to pursue this approach further. This project is an initial attempt to the study the role of the MPC in A549 tumour cell biology and the results highlight the importance of MPC in both cell respiration and proliferation.