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Figure 1 | Molecular Cancer

Figure 1

From: CD133 facilitates epithelial-mesenchymal transition through interaction with the ERK pathway in pancreatic cancer metastasis

Figure 1

CD133+pancreatic cancer cells were prone to generating metastatic nodules in in vivo models using immunodeficient mice. (A) Tumor morphologies (left) and CD133 immunohistological staining (right) of these tumors, which were observed in the pancreas at 4 weeks after the orthotopic implantation of Capan1M9 (CD133high) or shCD133M9 (CD133KD) cells. (B) Macro-metastatic nodules were observed in the lungs 16 weeks after the intravenous injection of Capan1M9 cells into the tail vein (left). The nodule was barely visible after the injection of shCD133M9 cells (right). (C) Macro-metastatic nodules observed in the liver at 4 weeks after the splenic implantation of Capan1M9 cells (left). In contrast, the metastatic nodule was barely visible after the implantation of shCD133M9 cells (right). (D) Statistical analysis of the number of macro-metastatic nodules generated in the lungs or liver after intravenous or splenic implantation showed that Capan1M9 cells were prone to generating metastases in comparison with shCD133M9 cells. Each mouse received 2 × 105 cells of Capan1M9 or shCD133M9 in these experiments.

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