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. 2023 Jun 1;19(6):e1010770. doi: 10.1371/journal.pgen.1010770

Fig 9. Evaluating for mechanisms of chemotherapy resistance due to clock dysfunction.

Fig 9

Gemcitabine resistance mechanism: A. Fold change in expression between KPC-BKO and KPC for channel protein hENT1 (SLC29A1 gene) and deoxycytidine kinase (DCK gene) is shown, with negative values representing downregulation in the KPC-BKO (clock disrupted) cells. B. CYCLOPS reordered samples (0 to 2π) from normal (n = 50) and pancreatic ductal adenocarcinoma (n = 318) is depicted for each of the respective genes from (A), demonstrating arrhythmic gene expression in human normal and pancreas cancer tissue. Shading around the blue regression line indicates the 95% confidence interval. Paclitaxel resistance mechanism: C. Fold change in expression between KPC-BKO and KPC for ATP-binding cassette drug efflux transporters (Abcb1a and Abcb1b genes) are shown, with negative values representing downregulation in the KPC-BKO (clock disrupted) cells. D. CYCLOPS reordered samples (0 to 2π) depict the human ABCB1 gene expression in normal (rhythmic) and PDAC (arrhythmic and suppressed) tissue. Shading around the blue regression line indicates the 95% confidence interval. p < 0.05, rAMP > 0.1, goodness of fit (rsq) > 0.1, and fitmean > 16 were considered rhythmic for CYCLOPS analysis [27].