Fig. 3 | Leukemia

Fig. 3

From: Oncogenic activation of JAK3-STAT signaling confers clinical sensitivity to PRN371, a novel selective and potent JAK3 inhibitor, in natural killer/T-cell lymphoma

Fig. 3

PRN371 effectively reduces the viability of NKTL cells by suppressing JAK3-mediated signaling. a Immunoblots of total and phosphorylated JAK3, STAT5, and STAT3 demonstrating constitutive activation of the JAK3-STAT signaling in NKTL. b IC50 of PRN371 and tofacitinib was determined by cell viability assays using 2-fold dilution series ranging from 10 nM to 10 μM concentration. The asterisk indicates cell lines that harbor STAT3-activating mutations. Western blot analysis of total and phosphorylated JAK3, STAT5, and STAT3 levels in NK92 and KAI-3 cells treated with the indicated concentrations of c PRN371 or d tofacitinib. Cells were cultured overnight without IL-2 and stimulated with IL-2 for 2 h with or without the indicated drug

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