Reciprocal Activation Between PLK1 and Stat3 Contributes to Survival and Proliferation of Esophageal Cancer Cells

Article ID	Journal	Published Year	Pages	File Type
3293322	Gastroenterology	2012	13 Pages	PDF

Abstract

Stat3 and PLK1 control each other's transcription in a positive feedback loop that contributes to the development of ESCC. Increased activity of Stat3 and overexpression of PLK1 promote survival and proliferation of ESCC cells in culture and in mice.

Keywords

STAT3 sis-inducible element PLK1 p-STAT3 ESCC shRNA eGFP FITC Janus kinase Small interfering RNA short hairpin RNA SiE siRNA Electrophoretic mobility shift assay standard deviation chromatin immunoprecipitation terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling Transcriptional regulation TUNEL standard error of mean subcutaneously EMSA یا electrophoretic mobility shift assay Signaling dominant negative phosphorylated STAT3 fluorescein isothiocyanate signal transducer and activator of transcription 3 SEM Cell death Neoplasm polymerase chain reaction PCR enhanced green fluorescent protein Polo-like kinase 1 JAK CHiP Esophageal squamous cell carcinoma