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Figure 4 | BMC Cancer

Figure 4

From: Therapeutic potential of PRL-3 targeting and clinical significance of PRL-3 genomic amplification in gastric cancer

Figure 4

Anticancer activity of PRL-3 inhibitor. (A) Proliferation assay after treatment with PRL-3 inhibitor at concentrations ranging from 0 to 50 μmol/L against 6 cell lines with different PRL-3 expression and genetic status. With cells treated with chemical solution alone (0 μmol/L PRL-3 inhibitor) as 1.0, the relative proliferative rate on 5 days after treatment was shown in left panel. The proliferative activity of AZ521 cells on 1, 2, 3, or 4 days after treatment was shown in right panel. L, low expression; H, high expression; D, disomy; P, polysomy; A, amplification; IC50, the 50% inhibitory concentration. (B) Anchorage-independent colony formation assays. Representative pictures of colony formation on AZ521 cells (top panel) and the relative rate of colony number (bottom panel) were shown. Bars, 200 μm; EC50, the 50% effective concentration. (C) Invasion assay. Representative pictures (top panel) and the relative invasive rate (bottom panel) were shown. Bars, 200 μm; *, P < 0.05 by Student t test, compared with 0 μmol/L of PRL-3 inhibitor; error bars, SD.

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