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Fig. 6 | Journal of Hematology & Oncology

Fig. 6

From: Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms

Fig. 6

In vivo effect of NiPT on KBM5- and KBM5R cell-derived mouse xenograft models. Nude mice bearing wild type and T315I-mutant Bcr-Abl xenograft tumors were treated with either vehicle or NiPT (2.5 mg/kg/day) for 11–14 days after inoculation of KBM5 and KBM5R cells. a NiPT inhibits tumor growth in vivo. Tumor growth curves were recorded every day in two sets of experiments. Mean ± SD (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001, versus NiPT-treated group. b On day 14 after inoculation, the mice were sacrificed, and the tumor tissues were weighed and imaged. ***P < 0.001, versus control group. c, d Western blot analyses (c) and/or immunohistochemistry staining for proteasome substrates (ubiquitinated proteins, p27), Bcr-Abl-related proteins (Bcr-Abl, p-Bcr-Abl) and its downstream proteins (Stat5, p-Stat5, Akt, Erk, p-Erk), and protein biomarkers related to proliferation (Ki-67), differentiation (CD11b/c), and adhesion and migration (CXCR4) in the xenograft tumor tissues from the KBM5 vehicle group (#2, 5, 6), KBM5 NiPT-treated group (#27, 28, 29), KBM5-T315I vehicle group (#16, 18, 19), and KBM5R-T315I NiPT-treated group (#35, 36, 37). In panel d, the proteins of interest are immunostained brown. All the immunohistochemical stainings were repeated in three mouse tumor tissues and the representative images are shown

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