Title : Signal transducer and activator of transcription 3 as molecular therapy for non-small-cell lung cancer.

Pub. Date : 2014 Apr

PMID : 24736071






4 Functional Relationships(s)
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1 METHODS: EGFR wild-type NSCLC cell lines (A549 H292 H322 H358 and H460) were treated with sorafenib or SC-1, a sorafenib derivative that closely resembled sorafenib structurally but was devoid of kinase inhibitory activity. Sorafenib transcription factor 19 Homo sapiens
2 METHODS: EGFR wild-type NSCLC cell lines (A549 H292 H322 H358 and H460) were treated with sorafenib or SC-1, a sorafenib derivative that closely resembled sorafenib structurally but was devoid of kinase inhibitory activity. Sorafenib transcription factor 19 Homo sapiens
3 SC-1 reduced STAT3 phosphorylation at tyrosine 705 in all tested EGFR wild-type NSCLC cells. Tyrosine transcription factor 19 Homo sapiens
4 Sorafenib and SC-1 enhanced Src homology-2 containing protein tyrosine phosphatase-1 (SHP-1) activity, whereas knockdown of SHP-1, but not SHP-2 or protein-tyrosine phosphatase 1B (PTP-1B), by small interference RNA reduced SC-1-induced apoptosis. Sorafenib transcription factor 19 Homo sapiens