Fig. 1: cNEK6 promotes gemcitabine chemotherapy resistance in PDAC.

A Venn diagram showing the intersection of differentially expressed circRNAs among the three gene sets. B Relative RNA levels of cNEK6 and NEK6 after actinomycin D treatment at different time points (n = 3) (RT-qPCR). C RT-qPCR was used to analyze the expression of cNEK6 and NEK6 after RNase R treatment of PANC-1 and PaTu8988t cells (n = 3). D Subcellular localization of cNEK6 detected by fluorescence in situ hybridization (FISH). Scale bars = 5 μm. E. Expression levels of cNEK6 between gemcitabine-resistant groups (PANC-1 GR and PaTu8988t GR) and their control groups (PANC-1 WT and PaTu8988t WT) (n = 3). F–H Effect of cNEK6 on the proliferative ability (IC50 (F), cell viability (G), and colony formation (H)) of gemcitabine-resistant groups (PANC-1 GR and PaTu8988t GR) and their control groups (PANC-1 WT and PaTu8988t WT) treated with gemcitabine (n = 3). I–K Schematic representation of the treatment regimen for patient-derived tumor xenograft (PDX) models (I) (n = 5). Xenografts were isolated and measured after euthanasia (J, K). L. CircRNA in situ hybridization (ISH) for cNEK6 in PDAC tissues. Scale bars = 100 μm (n = 20). M Kaplan–Meier analysis of overall survival and progression-free survival of patients with PDAC based on the expression of cNEK6.