Description
In this study, we found that kinase-dead IKK knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKK downregulation and marked pulmonary inflammation.KK downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKK-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKlowK5+p63hi cell transition to tumor cells in L-IkkKA/KA lungs. To further investigate the underlying mechanisms by which the lung SCC development, we generated two cell lines, named as S1 and S2 individually, which were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype. The aim of this microarray assay is to identify differentially expressed genes between S1 and S2 cells, which may highlight the important genes or pathways involved in inflammation-associated lung SCC carcinogenesis.