Aims: Recently, we reported the expression of functional membrane androgen receptors (mARs) in colon tumors inducing profound apoptotic tumor regression in vitro and in vivo. In the present study we analyzed mAR-induced downstream effectors controlling cell survival and the migratory potential of colon tumor cells. Methods: Western Blotting was performed to identify phosphorylated Akt, Bad, Focal adhesion kinase (FAK) and vinculin in Caco2 colon tumor cells. The migratory capacity of Caco2 cells was determined from matrigel and wound healing assays. Further experiments were performed in mice deficient in APC (apc^+/­) and in their wild type litter mates. Results: Activation of mAR downregulated the activity of Akt and induced long-term de-phosphorylation of Bad in Caco2 cells. Moreover, colon tumor tissues isolated from testosterone-conjugate-treated apc^+/­ mice expressed significantly lower p-Akt and p-Bad levels, as compared to colon tumor specimens from untreated mice. In line with this, the tumor incidence in APC-mice treated for 8 weeks with testosterone-conjugates was reduced by 80%. Furthermore, mAR activation in Caco2 cells strongly inhibited the migration potential of the cells. In accordance with this, vinculin and FAK, two proteins controlling cell adhesion and actin organization, were effectively phosphorylated upon mAR activation. Blocking actin reorganization by cytochalasin B restored the migration potential. Conclusion: mAR activation inhibits the pro-survival signals Akt/Bad in vitro and in vivo and blocks the migratory capacity of colon cancer cells via vinculin/FAK activation, supporting the important tumorostatic character of those receptors.