Abstract: Objective To investigate the role of PI3K／Akt／mTOR signaling pathway in epirubicininduced apoptosis and antiproliferation of human Tcell lymphoma cell line Jurkat. Methods The effects of 0， 1.25， 2.5， 5， 10μmol／L epirubicin and 0， 0.25， 0.5， 1， 2μmol／L dual PI3K／mTOR inhibitor（NVP-BEZ235） on human Tcell lymphoma cell line Jurkat proliferation after 48h was assessed by CCK8. The apoptosis of Jurkat cells with 0， 1.25， 2.5， 5， 10μmol／L epirubicin after 48h，5μmol／L epirubicin and 2μmol／L NVPBEZ235 after 0， 12， 24， 36 and 48h was detected by Annexin Ⅴ／PE double staining flow cytometry. The effects of 5， 10μmol／L epirubicin at 0， 6， 12， 24， 48h and the change of combining 2μmol／L NVPBEZ235 at 24, 48h with 5μmol/L epirubicin on the expressions of Akt, p-Akt, mTOR, pmTOR, p70s6k and pp70s6k were detected by Western blotting method. Results Epirubicin could inhibit proliferation of Jurkat cells and induce its apoptosis. When Jurkat was treated by 5μmol／L epirubicin， the apoptosis rate was 57.72％. The apoptotic effect was concentrationdependent. Epirubicininduced apoptosis of Jurkat cells was along with the changes of Akt， mTOR， p70s6k and their phosphorylation levels. NVPBEZ235 reduced the phosphorylation levels of Akt and p70s6k in Jurkat cells， which significantly improved the apoptosis of Jurkat cells. The apoptotic rate rose from 57.72％ to 78.31％ because of 2μmol／L NVPBEZ235 combining with 5μmol／L epirubicin after 48h. Conclusion Epirubicininduced apoptosis of Jurkat cells has a relation with PI3K／Akt／mTOR signaling pathway， when the pathway inhibitors combined with epirubicin， the cells sensitivity of epirubicin has improved to some extent.