Activation of the signal transducers and activators of the transcription 3 pathway in alveolar epithelial cells induces inflammation and adenocarcinomas in mouse lung

Yuan Li, Hong Du, Yulin Qin, Jennifer Roberts, Oscar W. Cummings, Cong Yan

Research output: Contribution to journalArticle

107 Scopus citations


The lung is an organ for host defense to clear up pathogens through innate and adaptive immunity. This process involves up-regulation of proinflammatory cytokines and chemokines that lead to activation of the signal transducers and activators of the transcription 3 (Stat3) signaling pathway. Overexpression of Stat3C in alveolar type II epithelial cells of CCSP-rtTA/(tetO) 7-Stat3C bitransgenic mice leads to severe pulmonary inflammation, including immune cell infiltration and upregulation of proinflammatory cytokines and chemokines in the lung. As a consequence, spontaneous lung bronchoalveolar adenocarcinoma was observed in bitransgenic mice. Aberrantly expressed genes in the bitransgenic model were identified and served as biomarkers for human bronchoalveolar adenocarcinoma. During tumorigenesis, genes that are critical to epithelial cell proliferation in lung development were reactivated. Therefore, Stat3 is a potent proinflammatory molecule that directly causes spontaneous lung cancer in vivo.

Original languageEnglish (US)
Pages (from-to)8494-8503
Number of pages10
JournalCancer Research
Issue number18
StatePublished - Sep 15 2007


ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this