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• W2164678001 abstract "// Sara Granja 1,2,* , Ibtissam Marchiq 3,* , Renaud Le Floch 3 , Conceição Souto Moura 5,6 , Fátima Baltazar 1,2,* and Jacques Pouysségur 3,4,* 1 Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal 2 ICVS/3B’s-PT Government Associate Laboratory, Braga/ Guimarães, Portugal 3 Institute for Research on Cancer and Aging of Nice (IRCAN), Centre A. Lacassagne, Nice, France 4 Centre Scientifique de Monaco (CSM), Monaco 5 Department of Pathology, Centro Hospitalar de São João, Porto, Portugal 6 Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP) and Medical Faculty of University of Porto, Porto, Portugal * These authors contributed equally to this work Correspondence to: Fátima Baltazar, email: // Jacques Pouysségur, email: // Keywords : lung cancer, CD147, BASIGIN, monocarboxylate transporters, MCTs, lactate, glycolytic metabolism, metformin, ZFNs Received : June 25, 2014 Accepted : December 02, 2014 Published : December 03, 2014 Abstract Most cancers rely on aerobic glycolysis to generate energy and metabolic intermediates. To maintain a high glycolytic rate, cells must efficiently export lactic acid through the proton-coupled monocarboxylate transporters (MCT1/4). These transporters require a chaperone, CD147/BASIGIN (BSG) for trafficking to the plasma membrane and function. To validate the key role of these transporters in lung cancer, we first analysed the expression of MCT1/4 and BSG in 50 non-small lung cancer (NSCLC) cases. These proteins were specifically upregulated in tumour tissues. We then disrupted BSG in three NSCLC cell lines (A549, H1975 and H292) via ‘Zinc-Finger Nucleases’. The three homozygous BSG -/- cell lines displayed a low MCT activity (10- to 5-fold reduction, for MCT1 and MCT4, respectively) compared to wild-type cells. Consequently, the rate of glycolysis, compared to the wild-type counterpart, was reduced by 2.0- to 3.5-fold, whereas the rate of respiration was stimulated in BSG -/- cell lines. Both wild-type and BSG-null cells were extremely sensitive to the mitochondria inhibitor metformin/phenformin in normoxia. However, only BSG-null cells, independently of their LKB1 status , remained sensitive to biguanides in hypoxia in vitro and tumour growth in nude mice. Our results demonstrate that inhibiting glycolysis by targeting lactic acid export sensitizes NSCLC to phenformin." @default.
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• W2164678001 date "2014-12-03" @default.
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• W2164678001 title "Disruption of BASIGIN decreases lactic acid export and sensitizes non-small cell lung cancer to biguanides independently of the LKB1 status" @default.
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• W2164678001 doi "https://doi.org/10.18632/oncotarget.2862" @default.
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