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STAT1, which carries tumor suppressor functions in several models, consists of two isoforms, namely STAT1 α  and STAT1 β . The biological function and significance of STAT1 β  has never been examined in human cancer. We examined STAT1 β  function in esophageal squamous cell carcinoma (ESCC) by transfecting a STAT1 β  gene into various ESCC cell lines. The interaction between STAT1 α  and STAT1 β  was examined by using co-immunoprecipitation and confocal microscopy. The prognostic significance of STAT1 β  expression, detectable by immunohistochemistry and western blot, was evaluated in a large cohort of ESCC patients. Enforced expression of STAT1 β  induced and prolonged the expression and phosphorylation of STAT1 α  in ESCC cells, and these effects were amplified by gamma-interferon (IFN- γ ). We also found that STAT1 β  interacts with STAT1 α  and decreases STAT1 α  degradation by the proteasome. Moreover, STAT1 β  substantially increased the DNA binding and transcription activity of STAT1. STAT1 β  also sensitized ESCC cells to chemotherapeutic agents, including cisplatin and 5-flurouracil. Using western blot and immunohistochemistry, we found that STAT1 β  was frequently decreased in esophageal cancer, as compared to their adjacent benign esophageal epithelial tissue. Loss of STAT1 β  significantly correlated with lymph node metastasis, invasion and shorter overall survival in ESCC patients. Therefore, STAT1 β  plays a key role in enhancing the tumor suppressor function of STAT1 α , in ESCC, in a manner that can be amplified by IFN- γ .

STAT1β enhances STAT1 function by protecting STAT1α from degradation in esophageal squamous cell carcinoma