PTP1B inhibitor promotes lysosomal degradation of Bcr-Abl. A, TonB.210 cells were untreated (lane 1) or treated with DOX for 48 h, resulting in the expression of Bcr-Abl (lanes 2–7). Cells were treated with 35 μm of the PTP1B inhibitor for 2 h (lane 3) or lactacystin (Lact, lane 4), chloroquine (CQ, lane 5), or PTP1B inhibitor (∅, PTP1B) for 2 h in addition to pretreatment with lactacystin (lane 6) or chloroquine (lane 7). Protein lysates were analyzed for Bcr-Abl, Tyr(P) (pY), and GAPDH by Western blot. B, cells were analyzed for intracellular ROS levels as measured by 2,7-dichlorodihydrofluorescein diacetate fluorescence on the FL-1 channel of a flow cytometer. The histogram shows relative fluorescence of treated cells in comparison with control cells. The data represent the mean ± S.D. of four independent experiments. UT, untreated.