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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Int J Cancer. 2011 Apr 25;130(3):509–520. doi: 10.1002/ijc.26005

Figure 4. Ectopic HA-MKK4 specifically inhibits Mat-Lu and AT3.1 metastatic colonization.

Figure 4

A. Biochemical characterization of Mat-Vector, Mat-Lu-HA-MKK4, AT3.1-Vector and AT3.1-HA-MKK4 cell lines. Left: Lysates of three independent Vector and HA-MKK4 clones from each cell line were immunoblotted (IB) for the expression of a HA-tagged protein, p38, and JNK. Actin was used as a loading control. Right: Kinase assays (KA) showing functionality of ectopically expressed HA-MKK4. B. Representative gross pathology of lungs harvested at 21 dpi from mice injected via tail vein with Mat-Lu-Vector and Mat-Lu-HA-MKK4 cells. C. Box plot representation of the mean number ± standard error of the mean of overt surface experimental metastases formed by Mat-Lu-Vector was 25.3 ± 7.7 as compared to 4 ± 1.4 for Mat-Lu-HA-MKK4 cells (p=0.045). D. Kaplan-Meier survival analyses showed that the median survival for Mat-Lu-Vector animals was 19 days vs. 25 days for Mat-Lu-HA-MKK4 animals (p<0.0001). E. Representative gross pathology of lungs harvested at 21 dpi from mice injected with AT3.1-Vector and AT3.1-HA-MKK4 cells. F. Box plot representation of the mean number ± standard error of the mean of overt surface metastases formed by AT3.1-Vector was 38.3 ± 7.6 as compared to 2.3 ± 1.1 for AT3.1-HA-MKK4 cells (p<0.001). G. Kaplan-Meier survival analyses showed that the median survival for AT3.1-Vector animals was 20 days vs. 27 days for AT3.1-HA-MKK4 animals (p<0.0001).