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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Hypoxia-induced exosomal circPDK1 promotes pancreatic cancer glycolysis via c-myc activation by modulating miR-628-3p/BPTF axis and degrading BIN1

Fig. 2

Exosomal circPDK1 is activated by HIF1A under hypoxic conditions. A The correlation between circPDK1 and PDK1 expression in 110 PC tissue samples. B The relative expression of circPDK1 and PDK1 mRNA in 7 PC cell lines. C The HIF1A protein level in PC cells exposed to different time under hypoxia (left) and circPDK1 expression level in PC cells exposed to indicated time in hypoxia (right). D The circPDK1 expression level in PC hypoxic exosomes exposed to indicated time in hypoxia. E The correlation between circPDK1 and HIF1A expression in 110 PC tissue samples. F The expression of HIF1A in PC tumor tissues and matched normal tissues verified by IHC assays in tissue microarrays. Scale bar = 1000 μm. G The correction of circPDK1 and HIF1A protein level was verified by IHC assays in tissue microarrays. H Upper schematic represents host gene PDK1 HREs obtained from JASPAR database. Dual-luciferase reporters were constructed with either of the two putative PDK1 HREs and matched mutant HREs in the PDK1 promoter region. I The luciferase intension of 293 T cells co-transfected with indicated luciferase reporter plasmids under hypoxia or loss of HIF1A. J ChIP assays were performed to assess the HREs interactions with the PDK1 promoter region. K The HIF1A protein levels in PC cells treated with indicated treatments. L, M The circPDK1 expression levels in PC cells treated with indicated treatments. N ChIP assays were performed to detect the binding strength between Pol II and the host gene PDK1 promoter in MIA PaCa-2 cells and normoxia and hypoxia. O The circPDK1 expression levels in MIA PaCa-2 cells treated with ActD (1 μg/mL) followed by indicated treatments. *P < 0.05; **P < 0.01; ***P < 0.001; ns, no significance

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