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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 5. Transient suppression of metastatic colonization imparted by MKK4 not due to clonal loss or dysfunction of HA-MKK4 construct.

Figure 5

A. Non-linear regression analysis of overt surface lung lesions as a function of time. Each point represents the mean ± SEM surface metastases from a minimum of 5 animals per time point. The Adjusted R2=0.67. The calculated t0 delay for the AT6.1-HA-MKK4 curve is 15.7 days relative to the AT6.1-Vector curve. B. Representative immunoblots (top) from>30 AT6.1-MKK4 overt experimental metastases and (bottom) from multiple independent metastasis derived cell lines (MDLs) demonstrating presence of HA-MKK4 construct within overt metastases and MDL’s. C. Representative in vitro kinase assay (top) AT6.1-MKK4 overt metastases and (bottom) from multiple independent metastasis derived cell lines (MDLs) showing inactive HA-MKK4 kinase within overt metastases; however HA-MKK4 remains functionally intact and activatable in cell lines derived from overt metastases. D. Persistent suppression of metastatic colonization at 28 DPI with MDL’s. The mean and SEM for surface metastases were 80.5±9.7 for Vector, 19.8±6.3 for HA-MKK4 parental, and 19.4±3.5 for HA-MKK4 MDLs (p=0.97, MDL versus parental AT6.1-vector p<0.0001).