Background & objective: Tumor microenvironment affects tumor cells growth. Bone marrow microenvironment may protect leukemic cells from drug-induced damages, but the mechanism is unclear. This study was to explore the protection of bone marrow stromal cells (BMSCs) on leukemic cells against chemotherapy and its mechanism.
Methods: Normal and leukemic BMSCs were isolated using Percoll, and cocultured with human acute lymphocyte leukemic cell line Jurkat cells in vitro. After treatment of 0.5 micromol/L of daunorubicin (DNR), apoptosis and cell cycle distribution of Jurkat cells were analyzed by flow cytometry.
Results: When treated with DNR for 24 h, apoptosis rate of normal BMSCs-cocultured Jurkat cells was significantly lower than that of Jurkat cells without coculture [(8.39+/-4.08)% vs. (16.02+/-1.00)%, P < 0.05], and apoptosis rate of leukemic BMSCs-cocultured Jurkat cells was significantly lower than that of normal BMSCs-cocultured Jurkat cells [(5.73+/-1.78)% vs. (8.39+/-4.08)%, P < 0.05]; G(0)/G(1) phase percentage of BMSCs-cocultured Jurkat cells was significantly higher than that of Jurkat cells without coculture (P < 0.05), but the difference between Jurkat cells cocultured with normal and leukemic BMSCs was not significant (P > 0.05).
Conclusion: Leukemic BMSCs may inhibit DNR-induced apoptosis in leukemic cells partly through G(0)/G(1) phase arrest.