Fig. 6
CBX reduces the BM-MSC-induced chemoresistance of AML cells to cytarabine. Cocultures experiments of leukemic cells and BM-MSCs were performed for 48 h with CBX (150 µM) and/or Ara-C (1 µM). a CBX decreased the percentage of quiescent leukemic cells (G0 phase) in contact with BM-MSCs and did not reduce the percentage of cells actively engaged in the cell cycle (S, G2, and M phases), conversely to its effect on isolated leukemic cells (n = 5). b (Left) Ara-C and CBX reduced the adhesion of KG1a cells to normal BM-MSCs. The percentage of adherent KG1a cells (CD45+) was reduced after adding Ara-C and/or CBX to the coculture system (n = 5). b (Right) Normal BM-MSCs protected KG1a cells against the proapoptotic effect of Ara-C, and CBX treatment reduced BM-MSC-antiapoptotic protection. Apoptosis and necrosis were studied in CD45+ CD90− adherent KG1a cells (n = 5). c (Left) Ara-C and CBX reduced the adhesion of primary AML blast cells on normal BM-MSCs. The percentage of adherent leukemic cells (CD45+) was reduced after adding Ara-C and/or CBX to the coculture system (n = 5). c (Right) Normal BM-MSCs protected primary AML blast cells against the proapoptotic effect of Ara-C, and CBX treatment reduced BM-MSC-antiapoptotic protection. Apoptosis and necrosis were studied in CD45+CD90− adherent AML blast cells (n = 5). d (Left) Ara-C and CBX reduced the adhesion of KG1a cells on leukemic BM-MSCs. The percentage of adherent leukemic cells (CD45+) was reduced after adding Ara-C and/or CBX to the coculture system (n = 5). d (Right) Leukemic BM-MSCs protected KG1a cells against the proapoptotic effect of Ara-C, and CBX treatment reduced MSC-antiapoptotic protection. Results are expressed as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001
