Fig. 1: LCN2 is upregulated across several models of pancreatic cancer cachexia and correlates with food consumption and muscle loss.

a Cumulative food intake in five models of pancreatic cancer cachexia and sham operation controls. b Total food intake normalized to sham control group. c Skeletal muscle catabolism as indicated by terminal gastrocnemius mass normalized to body mass. d Cardiac muscle catabolism as indicated by terminal heart mass normalized to body mass. e Gastrocnemius, f heart, g hypothalamus, and h liver gene expression profiles in pancreatic cancer cachexia models (represented as relative quantity to sham control). Terminal i plasma and j CSF LCN2 levels. Linear regression analysis between plasma LCN2 levels and k total food intake or l gastrocnemius mass. Linear regression analysis between CSF LCN2 levels and m total food intake or n gastrocnemius mass. a–i, k, l N = 6 per group. j, m, n N = 6 per group except KPC (N = 4 per group). All data are expressed as mean ± SEM. Data represented in b–j were analyzed with one-way ANOVA with Bonferroni multiple comparisons comparing tumor experimental groups to sham operation control. k–n Analyzed by simple linear regression and two-tailed correlation analyses. *p ≤ 0.05, **p ≤ 0.01, and ***p ≤ 0.001, ****p ≤ 0.0001. Sham operation controls = gray/black, KPC = red, 4662 = blue, FC1199 = purple, FC1242 = orange, FC1245 = green.