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IKKα links inflammation and tumorigenesis in lung squamous cell carcinoma

Thursday, October 11, 2012 — Poster Session IV

2:00 p.m. – 4:00 p.m.

Natcher Conference Center, Building 45



* FARE Award Winner


  • Q Jiang
  • Z Xiao
  • J Willette-Brown
  • T Back
  • F Zhu
  • M Datla
  • RH Wiltrout
  • Y Hu


IkB Kinase subunitα (IKKα) mutations have been reported in many types of human cancer. Our recent study established a mouse model of lung squamous cell carcinoma (SCC) by inactivating IKKα in vivo. We here show that inactivation of IKKα in mice causes systemic whole-life chronic inflammation, which consequently promotes lung SCC initiation and progression. In mice with mutated IKKα, inflammatory cells and cytokines/chemokines are remarkably elevated in the lung. An M2 macrophage phenotype is observed only in the lungs of old IKKα mutant mice, not in younger mice, suggesting the M1/M2 polarization may be driven by the proinflammatory microenvironment in these mice. Production of Th2 cytokines and IL-10 are elevated in CD4 T cells from the lungs of mice with mutated IKKα, and may contribute to M2 polarization during the chronic inflammation. In addition, depletion of macrophages in these mice can significantly reduce Th2 cytokine production, oxidative DNA damage, and completely shut down SCC development. Taken together, our study generates, for the first time, a spontaneous mouse model of inflammation-associated lung SCC, and suggests that IKKα plays important roles in linking inflammation and carcinogenesis of lung squamous cell carcinoma.

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