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. 2016 Aug 23;8(52):89552–89565. doi: 10.18632/oncotarget.11533

Figure 3. Periostin promotes pancreatic cancer cell proliferation, migration, invasion, and clone formation.

Figure 3

(A and B) Periostin knockdown decreased the proliferation rate of SW1990 and BxPC-3 cells. In contrast, increased periostin expression accelerated the proliferation of SW1990 and BxPC-3 cells. OD at 450 nm was measured by CCK-8 assay at 0, 24, 48, 72, and 96 h and is shown as the mean ± SD. (C and D) Periostin knockdown inhibited migration and invasion of SW1990 and BxPC-3 cells, whereas increased periostin expression exerted the opposite effect. Cells were stained with crystal violet and observed by microscopy (×50 magnification; Zeiss). The number of migration or invasion cells in five random fields was counted by ImageJ software (×100 magnification; Zeiss) and is shown as the mean ± SD. (E) periostin knockdown inhibited the ability of SW1990 and BxPC-3 cells to form clonogenic colonies. Cells were stained with crystal violet and photographed without magnification and under light microscopy (×50 magnification; Zeiss). Bar charts show the number of colonies. (F) Periostin promoted wound healing in SW1990 and BxPC-3 cells. Cells were scraped with a p10 tip (time 0) and images were captured at the same time every day thereafter (×50 magnification; Zeiss). Migration distance was measured from five fields captured at each indicated time point. The percentage of wound repair for each cell line is shown using bar charts. *P < 0.05, **P < 0.01 and ***P < 0.01 vs. control shRNA.