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. 2016 Jan 15;30(2):233–247. doi: 10.1101/gad.263327.115

Figure 4.

Figure 4.

Activation of Prrx1a and suppression of Prrx1b foster metastatic colonization. (A) Experimental design for orthotopic transplantation using KPC2 control, Prrx1a-overexpressing, and Prrx1b-overexpressing cells. (B) Representative histology of liver metastases of KPC2 control, Prrx1a, and Prrx1b tumors. Bar, 100 μm. (C) Frequency of small/large liver metastases in three tumor groups. Small metastases contain <100 cancer cells, and large metastases contain >100 cancer cells. (D) Experimental design for intraportal vein injection (liver metastasis model) of KPC2 cells. (E, top and middle panels) Representative histology and IHC staining for E-CADHERIN (ECAD) in metastatic liver disease in three experimental groups. Bar, 100 μm. (Bottom panels) IHC staining for Ki-67 in three groups. Bar, 20 μm. (F) Frequency of small/large liver metastases in three groups. (G) Percentage of mice harboring large metastases. (H) Percentage of Ki-67-positive cells in each liver metastasis in three groups. n = 6 for each group. (I) Experimental design for orthotopic transplantation using KPC2-Prrx1a or KPC2-Prrx1b cells with or without doxycycline. (J) Representative histology of liver metastases. Bar, 100 μm. (K) Frequency of liver metastases in four experimental groups (on/off Prrx1a or Prrx1b). Doxycycline treatment was initiated 12 d after transplantation. (L) Frequency of large metastases in four experimental groups.