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. 2012 Feb 23;103(4):739–746. doi: 10.1111/j.1349-7006.2012.02214.x

Figure 2.

Figure 2

(A) The results of coimmunoprecipitation assay in pancreatic cancer cell line PK9 and clinical samples from the patients with pancreatic ductal adenocarcinoma. The whole cell lysates extracted from cell line or tissue homogenates extracted from two surgical specimens were immunoprecipitated and immunoblotted with anti‐MUC16 and anti‐mesothelin antibody. IB, immunoblotting. (B) Invasion chamber experiments in PK9 transfected with MUC16 shRNA. The invasion was significantly suppressed after inhibition of MUC16 expression (*P = 0.0009, **P = 0.0067). (C) Migration assays in PK9 transfected with MUC16 shRNA. The migration was significantly suppressed after downregulation of MUC16 expression (*P = 0.0005, **P = 0.0055). (D) Invasion assay with the blockage of MUC16 binding to mesothelin with the neutralizing antibodies against MUC16 (OC125 or M11, *P = 0.0014, **P = 0.0043). (E) Migration assay with the blockage of MUC16 binding to mesothelin with OC12 5 or M11 (*P = 0.0020, **P = 0.0003). (F) Cell growth assay in PK9 transfected with MUC16 shRNA. The cell growth was significantly suppressed after inhibition of MUC16 expression (*P = 0.0469, **P = 0.0036). NS, not significant.