FIGURE 5.

Galunisertib treatment promotes EMT to MET phenotypic conversion in prostate tumors in vivo. Panel A shows representative images of E-cadherin and N-cadherin immunostaining in serial sections of prostate tumors from vehicle control and galunisertib-treated mice, given as a single agent (magnification, ×400). Panel B shows the results of Western blot analysis of expression profile of EMT protein effectors E-cadherin and N-cadherin in total cell lysates of prostate tumors from vehicle control, and inhibitor treated as monotherapy and combination of galunisertib and enzalutamide in DNTGFβRII mice. GAPDH was used as a loading control. Panel C indicates the ratio of relative expression of E-Cadherin over N-cadherin in prostate tumor cell lysates from the Western blot analysis and subsequent densitometric analysis of protein bands for each respective protein. TGFβRI inhibitor led to an increase in E-cadherin paralleled by increased N-cadherin protein levels in prostate tumors (favoring MET reversal of TGF-β-mediated EMT in response to galunisertib). Values represent the mean intensity of bands from samples from the three treatment mini-trials ± SEM.