Figure 4
Inhibition of Hsp90 activity in INA-6 and ANBL-6 cells by 17-DMAG attenuates levels of phosphorylated and total STAT3 and phosphorylated ERK1,2 and induces apoptosis also in the presence of cells from the BMM. (A) Western blot analysis of phosphorylated (Y705) and total STAT3 and of phosphorylated and total ERK1,2 in INA-6 or ANBL-6 cells that were treated with different concentrations of 17-DMAG for 20 hours. Staining of β-actin served as a loading control. (B-C) Viability analysis of 17-DMAG–treated INA-6 or ANBL-6 cells. INA-6 or ANBL-6 cells were kept either in medium with 2 ng/mL IL-6 (B) or cultured in the presence of BMSCs, OCs or HUVECs (C) and treated with different concentrations of 17-DMAG for 3 days. The viable fractions of the treated cells were determined by annexin V–FITC/PI staining.

Inhibition of Hsp90 activity in INA-6 and ANBL-6 cells by 17-DMAG attenuates levels of phosphorylated and total STAT3 and phosphorylated ERK1,2 and induces apoptosis also in the presence of cells from the BMM. (A) Western blot analysis of phosphorylated (Y705) and total STAT3 and of phosphorylated and total ERK1,2 in INA-6 or ANBL-6 cells that were treated with different concentrations of 17-DMAG for 20 hours. Staining of β-actin served as a loading control. (B-C) Viability analysis of 17-DMAG–treated INA-6 or ANBL-6 cells. INA-6 or ANBL-6 cells were kept either in medium with 2 ng/mL IL-6 (B) or cultured in the presence of BMSCs, OCs or HUVECs (C) and treated with different concentrations of 17-DMAG for 3 days. The viable fractions of the treated cells were determined by annexin V–FITC/PI staining.

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