Effects of CXCL12 isoforms in a pancreatic pre-tumour cellular model: Microarray analysis

Figure 1 Hierarchical cluster heatmap of treated (α, β and γ isoforms) and control (C1, C2, C3) samples based on the obtained differentially expressed genes. Distance measurement method: Pearson; Clustering method: Average linkage.

Figure 2 Comparison of the number of differentially expressed genes in all treatment conditions (α, β and γ CXCL12 isoforms) in hTERT-HPNE cells. Differentially expressed genes were detected using an FDR-corrected P value threshold of P < 0.05.

Figure 3 Real-Time polymerase chain reaction analysis of differentially expressed genes. Expression levels of CXCL8, RRP12, ADH1B, UBA7, FEM1C, and CASP1 in treated and untreated hTERT-HPNE cells. All values are expressed as the mean ± SD. Values were considered to be significantly different respect to the control at ^aP < 0.05.

Figure 4 Migration ability of hTERT-HPNE cells. Wound healing assay was used to assess the effect of CXCL12 isoform treatments on cell migration. A: The cells were photographed immediately (0 h) after wounding by a pipette tip and at different time points (12 h and 24 h); B: The migration ability of the treated cells was evaluated by measuring their efficiency in wound repair compared with that of the control. All values are expressed as the mean ± SD. Values were considered to be significantly different respect to the control at ^aP < 0.05.