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Fig. 1 | Cancer & Metabolism

Fig. 1

From: Metabolic plasticity imparts erlotinib-resistance in pancreatic cancer by upregulating glucose-6-phosphate dehydrogenase

Fig. 1

Erlotinib-resistant cells display downregulated glycolysis. a Effect of erlotinib treatment (48 h) on the survival of erlotinib-sensitive (MiaPaCa2 and AsPC1) and erlotinib-resistant (MiaPaCa/Erlo and AsPC/Erlo) cells was analyzed using clonogenic assay (n = 3). b Representation of central carbon metabolism. c, d Immunoblot and real-time PCR analyses depicting glycolytic enzyme levels in drug-sensitive and drug-resistant cells. HK2, hexokinase 2; GPI, glucose phosphate-isomerase; PFK, phosphofructokinase; PKM, pyruvate kinase M; PGM, phosphoglycerate mutase; PGK, phosphoglycerate kinase; LDHA, lactate dehydrogenase A (n = 2) (n = 3). e The metabolic phenotype was assessed in cells using Seahorse metabolic analyzer. Graph showing ECAR (glycolysis) levels in sensitive and resistant cells (n = 3). f Pyruvate levels were assessed in cells using LC-MS analysis. Graph showing pyruvate levels relative to MiaPaCa2 cells (n = 2). Data presented as average ± SEM (*p < 0.05, #p < 0.01)

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