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. 2023 Aug 28;4(9):1326–1344. doi: 10.1038/s43018-023-00614-y

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Extended Data Fig. 1 — a. Prediction of LOX, LOXL1, 3 and 4 secondary structures based on the previously published secondary structure of LOXL2 (PDB ID: 5ZE3). Each family member contains a highly conserved catalytic domain critical to the formation of the active enzymatic site. LOXL2-4 contain four repeat scavenger receptor cysteine-rich (SRCR) domains (not identical sequences). LOX and LOXL1 contain additional cleavage sites and propeptide domains. b. Lysyl oxidases catalyze the oxidative deamination of lysine residues in the telopeptide regions of tropocollagen molecules resulting in the formation of reactive aldehydes which undergo spontaneous (blue) condensation to yield crosslinks. Further assembly of these tropocollagen molecules results in fibrillar collagen. c, d. Forest plots for lysyl oxidase family members showing hazard ratios for each individual family member and combined ‘lysyl oxidase family’ scores in the APGI/ICGC n = 269 patients (C) and TCGA n = 178 patients (D) cohorts. Cox proportional hazards model; dots indicate the hazard ratio and whiskers the 95% confidence interval. e, f. Distribution of lysyl oxidase family scores according to tumor stage in the APGI/ICGC (E) and TCGA (F) cohorts. g, h. Patient stratification by molecular subtype according to lysyl oxidase family score in the APGI/ICGC (G) and TGCA (H) cohorts. p value determined by Kruskal-Wallis (Nonparametric One-Way ANOVA) and unpaired, nonparametric t-test with a Mann–Whitney U correction (comparison between two groups) i. Quantification of bulk modulus (stiffness) by unconfined compression testing in age-matched healthy pancreas and KPC PDAC tumors (n = 5 animals per group), p value determined by unpaired, nonparametric t-test with a Mann–Whitney U correction (comparison between two groups). Data presented as mean values +/− SD. j. Schematic of bulk compression testing on cross-sectional slices of samples k. Immunoblot analysis of LOX from corresponding age-matched healthy pancreas and PDAC tumors (n = 5 animals per group) and corresponding ponceau stain as loading control. l. CAFs and CCs derived from the Pdx1-Cre; LSL-Kras^G12D/+; LSL-p53^R172H/+ (KPC) model (sorted by FACs) as previously described⁴⁶.

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