Autophagy is a process of cellular self-digestive pathway that degrades organelles and accumulated protein aggregates. Due to the promiscuous role of autophagy in the viability and death of tumor cells, its effect on lung cancer cells remained to be clarified. Atg13 is essential for autophagy induction and cells deficient of this protein are characterized by a firmly compromised autophagic activity. In the present study, our main objective was to elucidate the mechanism by which autophagy regulates cell proliferation through Atg13. Using NSCLC, U1810 and A549 cell lines as models, we found that silencing of Atg13 significantly inhibited the proliferation of cells. Furthermore, changes in the distribution of cell cycle and the expression levels of cell cycle related proteins were assessed. In this regard, we showed that the cell cycle distribution was not affected in cells transduced with shRNA targeting Atg13; however, reduction of Atg13 was associated with repression of cyclin A levels. Eventually, in response to DNA damage induced by therapeutic drugs, cells were arrested in the G2 phase indicating the increased sensitivity of Atg13 deficient cells to such drugs. In conclusion our data propose a mechanism that connect Atg13 and cell proliferation in lung cancer cells.