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Fig. 1 | Cancer & Metabolism

Fig. 1

From: Glucagon signaling via supraphysiologic GCGR can reduce cell viability without stimulating gluconeogenic gene expression in liver cancer cells

Fig. 1

HCC cell lines are dependent on exogenous glucose/lipid dependency and express low levels of the glucagon receptor, GCGR. a Cell proliferation assays of two cell lines, SNU398 and Huh7, at the indicated time point and nutrient conditions. Data represents a single experiment with 3 biological replicates. Red dashed line denotes fold change of 1, which refers to the starting number of cells. b Simplified Glucagon/GCGR signaling transduction. GCGR: g-coupled glucagon receptor, Ac: adenyly cyclase, cAMP: cyclic adenosine monophosphate, PKA: protein kinase A, p-CREB: phosphorylated cAMP-response element binding protein. c ATP-based cell viability assay of HCC cell lines cultured across a wide range of glucose concentrations. Data points represent the average of 6 biological replicates. d ATP-based cell viability assay of HCC cell lines cultured across a wide range of oleic acid concentrations. Data points represent the average of 6 biological replicates. e Normalized RNA-seq values for GCGR in human HCC compared to normal liver. Data obtained from TCGA. ****: p < 0.0001, unpaired two-tailed t test. n = 50(normal) and 374(tumor). f qPCR mRNA expression of GCGR in HCC cell lines compared to Primary Human Hepatocytes (PHH). Data represent a single experiment with 3 biological replicates (3 separate RNA samples). ****p < 0.0001, ordinary one-way ANOVA with Dunnett’s multiple comparisons test. g Kaplan-Meier plot of overall survival probability between high and low GCGR expression in liver cancer patients. Graph was generated using the website: https://kmplot.com

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