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Figure 7 | Journal of Translational Medicine

Figure 7

From: Specific-detection of clinical samples, systematic functional investigations, and transcriptome analysis reveals that splice variant MUC4/Y contributes to the malignant progression of pancreatic cancer by triggering malignancy-related positive feedback loops signaling

Figure 7

qRT-PCR, western blotting, and ELISA verification of DEGs related to the malignant functions of MUC4/Y and VEGF family molecules. (A) Distribution of DEGs in the main pathways related to oncogenic transformation showing the change derived from MUC4/Y overexpression–associated molecular signatures; the proportions of each pathway (represented by different colors) are graphed. The DEG list for annotations is the intersection set of PANC-1-MUC4/Y compared to the controls; absolute value of log2 ratio ≥1. (B) Representative qPCR validation results of 44 DEGs and VEGF family molecules (VEGFA, B, C) in PANC-1-MUC4/Y and control cell. (C) Western blot analysis verified a significant upregulation of t-HER2/ErbB2, p-HER2/ErbB2, t-FAK, p-FAK, p-Src, p-AKT(Thr308), p-AKT(Ser473), p-IκBα, p-NF-kB, t-ERK, p-ERK, t-JNK, p-JNK, and p-C-JUN in PANC-1-MUC4/Y compared with control. (D) ELISA of VEGF and IL8/CXCL8 using cell culture supernatants. Left: VEGF; right: IL8/CXCL8 production from PANC-1–derived clones incubated for 24 h or 48 h. Bars denote mean ± SD, ***P <0.001, **P <0.01.

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