Cell migration is dependent on a series of integrated cellular events including 
the membrane recycling of the extracellular matrix receptor integrins. In this 
paper, we investigate the role of autophagy in regulating cell migration. In a 
wound-healing assay, we observed that autophagy was reduced in cells at the 
leading edge than in cells located rearward. These differences in autophagy were 
correlated with the robustness of MTOR activity. The spatial difference in the 
accumulation of autophagic structures was not detected in rapamycin-treated 
cells, which had less migration capacity than untreated cells. In contrast, the 
knockdown of the autophagic protein ATG7 stimulated cell migration of HeLa 
cells. Accordingly, atg3(-/-) and atg5(-/-) MEFs have greater cell migration 
properties than their wild-type counterparts. Stimulation of autophagy increased 
the co-localization of β1 integrin-containing vesicles with LC3-stained 
autophagic vacuoles. Moreover, inhibition of autophagy slowed down the lysosomal 
degradation of internalized β1 integrins and promoted its membrane recycling. 
From these findings, we conclude that autophagy regulates cell migration, a 
central mechanism in cell development, angiogenesis, and tumor progression, by 
mitigating the cell surface expression of β1 integrins.