δ-Catenin promotes cell migration and invasion via Bcl-2-regulated suppression of autophagy in prostate cancer cells.

As a member of the catenin family, δ-catenin is overexpressed in many cancers, including prostate cancer, and the role of δ-catenin in prostate tumor growth has been reported. However, the involvement of δ-catenin in the migration and invasion of prostate cancer has rarely been studied. In this study, we innovatively proposed that δ-catenin would enhance the migration and invasion ability of prostate cancer cells. It is worth noting that the molecular mechanism underlying the effect involved the downregulation of autophagy. We demonstrated that δ-catenin could suppress autophagy by Bcl-2-regulated disruption of the Beclin1-Vps34 autophagosome complex. Furthermore, the effect of δ-catenin on promoting cell migration and invasion was dependent upon β-catenin-mediated Bcl-2 transcription. Finally, using rapamycin and bafilomycin, we largely confirmed that the degradation of Snails by autolysosomes may be related to δ-catenin regulated migration and invasion. Overall, our results indicated that δ-catenin promoted cell migration and invasion of prostate cancer cells via Bcl-2-regulated autophagy suppression. AJCR