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Figure 4 | Journal of Translational Medicine

Figure 4

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 4

MUC4/Y enhances PANC-1 cell malignant activity in vitro . Data from three repeated experiments are presented as means ± SD. **P <0.01, ***P <0.001 vs. controls. (A) MUC4/Y enhanced in vitro proliferation of PANC-1 cells under stress from low nutritional status. The absorbance values of cells at different time points were detected with WST-8 dye. Cells were maintained in medium containing 10% serum (left) and 1% serum (right). (B) MUC4/Y increased resistance to apoptotic reagents, i.e., sorafenib. Representative templates of FACS analysis showing the proportion of cells positive for annexin V and 7-AAD (top right quadrant) representing the percentage of necrotic cells; the proportion of cells that were annexin V–positive and 7-AAD–negative (bottom right quadrant) represented the percentage of apoptotic cells (top). Bar denotes the percentage of apoptotic and necrotic cells in PANC-1–derived clones (bottom). (C) MUC4/Y affected pancreatic cancer cell metastatic potential in vitro. Bar graph shows the number of PANC-1–derived clones that had migrated or invaded through the Matrigel. (D) MUC4/Y enhanced cancer cell–associated HUVEC endotube formation. Bar denotes the fold increase of the number of endotubes compared to the blank control.

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Journal of Translational Medicine

ISSN: 1479-5876

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