Figure 5.
Figure 5. JAK2 inhibition leads to STATs dephosphorylation and apoptosis in cHL tumor cells carrying STAT6 or STAT3 mutations. (A) Western blot analysis of STAT6, STAT3, and STAT5 phosphorylation in L1236, L428, and HDLM2 cells analyzed 24 hours after treatment with the JAK2 inhibitor fedratinib (at the indicated concentrations) or with vehicle (dimethyl sulfoxide) as control (1 representative experiment per cell line is shown, of 3 independently performed, that gave reproducible results). Normalized levels of total STATs relative to β-tubulin, and of phospho-STATs relative to the corresponding total STATs, were quantified by densitometry and are shown below the respective blots. (B) Percentage of live cells (AnnexinV-negative by flow cytometry) in the same cell lines, measured 48 hours after treatment with fedratinib, relative to the vehicle set at 100%. Error bars (standard error of the mean) refer to 4 independent experiments, each done in duplicate; P values were computed by 2-way ANOVA.

JAK2 inhibition leads to STATs dephosphorylation and apoptosis in cHL tumor cells carrying STAT6 or STAT3 mutations. (A) Western blot analysis of STAT6, STAT3, and STAT5 phosphorylation in L1236, L428, and HDLM2 cells analyzed 24 hours after treatment with the JAK2 inhibitor fedratinib (at the indicated concentrations) or with vehicle (dimethyl sulfoxide) as control (1 representative experiment per cell line is shown, of 3 independently performed, that gave reproducible results). Normalized levels of total STATs relative to β-tubulin, and of phospho-STATs relative to the corresponding total STATs, were quantified by densitometry and are shown below the respective blots. (B) Percentage of live cells (AnnexinV-negative by flow cytometry) in the same cell lines, measured 48 hours after treatment with fedratinib, relative to the vehicle set at 100%. Error bars (standard error of the mean) refer to 4 independent experiments, each done in duplicate; P values were computed by 2-way ANOVA.

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