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We have recently shown a gender-specific role for epithelial Stat3 signaling in the pathogenesis of K-ras mutant LUAD. The absence of epithelial Stat3 in male K-ras mutant mice (LR\/Stat3\u0394\/\u0394 mice) promoted tumorigenesis and induced a nuclear factor-kappaB (NF-\u03baB)-driven pro-tumor immune response while reducing tumorigenesis and enhancing anti-tumor immunity in female counterparts. In the present study, we manipulated estrogen and NF-\u03baB signaling to study the mechanisms underlying this intriguing gender-disparity. In LR\/Stat3\u0394\/\u0394 females, estrogen deprivation by bilateral oophorectomy resulted in higher tumor burden, an induction of NF-\u03baB-driven immunosuppressive response, and reduced anti-tumor cytotoxicity, whereas estrogen replacement reversed these changes. On the other hand, exogenous estrogen in males successfully inhibited tumorigenesis, attenuated NF-\u03baB-driven immunosuppression and boosted anti-tumor immunity. Mechanistically, genetic targeting of epithelial NF-\u03baB activity resulted in reduced tumorigenesis and enhanced the anti-tumor immune response in LR\/Stat3\u0394\/\u0394 males, but not females. Our data suggest that estrogen exerts a context-specific anti-tumor effect through inhibiting NF-\u03baB-driven tumor-promoting inflammation and provide insights into developing novel personalized therapeutic strategies for K-ras mutant LUAD.<\/jats:p>","DOI":"10.1093\/carcin\/bgaa064","type":"journal-article","created":{"date-parts":[[2020,6,30]],"date-time":"2020-06-30T20:56:36Z","timestamp":1593550596000},"page":"1529-1542","source":"Crossref","is-referenced-by-count":18,"title":["Interplay between estrogen and Stat3\/NF-\u03baB-driven immunomodulation in lung cancer"],"prefix":"10.1093","volume":"41","author":[{"given":"Shanshan","family":"Deng","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Xi\u2019an Jiaotong University, Xi\u2019an, China"},{"name":"Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, 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