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Here we show that autophagy modulation regulates the migration and invasion capabilities of glioblastoma (GBM) cells. We observed that during autophagy occurrence, obtained by nutrient deprivation or by pharmacological inhibition of the mTOR complexes, GBM migration and chemokine\u2010mediated invasion were both impaired. We also observed that SNAIL and SLUG, two master regulators of the epithelial\u2013mesenchymal transition (EMT process), were down\u2010regulated upon autophagy stimulation and, as a consequence, we found a transcriptional and translational up\u2010regulation of N\u2010 and R\u2010cadherins. Conversely, in BECLIN 1\u2010silenced GBM cells, an increased migration capability and an up\u2010regulation of SNAIL and SLUG was observed, with a resulting decrease in N\u2010 and R\u2010cadherin mRNAs. ATG5 and ATG7 down\u2010regulation also resulted in an increased migration and invasion of GBM cells combined to an up\u2010regulation of the two EMT regulators. Finally, experiments performed in primary GBM cells from patients largely confirmed the results obtained in established cell cultures.<\/jats:p>\n                  <jats:p>Overall, our results indicate that autophagy modulation triggers a molecular switch from a mesenchymal phenotype to an epithelial\u2010like one in GBM cellular models. Since the aggressiveness and lethality of GBM is defined by local invasion and resistance to chemotherapy, we believe that our evidence provides a further rationale for including autophagy\/mTOR\u2010based targets in the current therapeutical regimen of GBM patients.<\/jats:p>","DOI":"10.1016\/j.molonc.2015.04.016","type":"journal-article","created":{"date-parts":[[2015,5,13]],"date-time":"2015-05-13T02:34:01Z","timestamp":1431484441000},"page":"1612-1625","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":269,"title":["Autophagy induction impairs migration and invasion by reversing EMT in glioblastoma 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