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      Therapeutic suppression of constitutive and inducible JAK\STAT activation in head and neck squamous cell carcinoma.

      Journal of experimental therapeutics & oncology

      Angiogenesis Inhibitors, pharmacology, Animals, Antineoplastic Agents, therapeutic use, Biotransformation, drug effects, Blotting, Western, Carcinoma, Squamous Cell, drug therapy, metabolism, pathology, Cell Line, Tumor, Cell Proliferation, Electrophoretic Mobility Shift Assay, Enzyme-Linked Immunosorbent Assay, Head and Neck Neoplasms, Immunohistochemistry, Indicators and Reagents, Male, Mice, Mice, Nude, Phosphorylation, Pyridines, STAT3 Transcription Factor, antagonists & inhibitors, biosynthesis, Signal Transduction, Tyrphostins, Vascular Endothelial Growth Factor A, genetics

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          The oncogenic role of STAT3 has been elucidated in a number of human malignancies including leukemia, lymphoma, malignant glioma and cancers of the breast, lung, and head and neck (HNSCC). Here we show that WP1066 has profound anti-neoplastic effects in HNSCC, mediated in part by suppression of JAK2-STAT3 signaling. WP1066 inhibited constitutive and inducible STAT3 phosphorylation in both dose- and time-dependant manners. Further, the nuclear translocation of STAT3 was completely inhibited, resulting in decreased DNA binding activity. In vivo testing of WP1066 in a nude mouse orthotopic model of HNSCC demonstrated significant anti-tumor effects, with histological evidence of decreased cellular proliferation and angiogenesis. Collectively, these data suggest that WP1066 suppresses squamous cell carcinoma cell growth, in part through its effects on JAK-STAT pathways, and establishes this small molecule as potentially efficacious agent in the treatment of HNSCC.

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