Figure 2 | Cell Death & Disease

Figure 2

From: Phosphorylation of signal transducer and activator of transcription 1 reduces bortezomib-mediated apoptosis in cancer cells

Figure 2

The suppression of STAT1 and JAK enhances bortezomib (BTZ)-induced cancer cells’ death. (a and b) The knockdown of STAT1 by short hairpin (sh)RNA and the treatment with 0.05 μM of BTZ for 24 h in TOV112D cells were analyzed by immunoblotting; specifically, the levels of caspase-3 cleavage were measured. Cytotoxicity was measured using the LDH assay. (c) Inhibition of the JAK/STAT pathway with JAKi I. (d) TOV112D cells were treated with 5 μM of JAKi I and 0.05 μM of BTZ for 24 h. Cell lysates were analyzed by immunoblotting to determine the levels of phosphorylated JAK1 and JAK1. (e) TOV112D cells treated with 0.05 μM of BTZ and 5 μM of JAKi I for 24 h were analyzed by immunoblotting to determine the levels of caspase-3 cleavage. (f) The cytotoxicity of the combined treatment with JAKi I and BTZ was measured using the Cell Death Detection ELISA in TOV112D cells. (g) LDH assays were used for the TOV112D, TOV21G, BR, and SKOV3 cells. (h) TOV112D cells were transiently transfected with enhanced green fluorescent protein (EGFP) alone (control vector) or EGFP-STAT1 (S727E) for 72 h, and then treated with 5 μM of JAKi and 0.05 μM of BTZ for 24 h. Cell viability was analyzed using the MTT assay. Data are expressed as mean±standard error of the mean. The results are representative of at least three independent experiments

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