Gene expression alteration by different cell lines derived from lung SCC of IKKM-NM-1 mutant mice

ABSTRACT: In this study, we found that kinase-dead IKKM-NM-1 knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKM-NM-1 downregulation and marked pulmonary inflammation.KKM-NM-1 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 IKKM-NM-1-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKM-NM-1lowK5+p63hi cell transition to tumor cells in L-IkkM-NM-1KA/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. There were two cell lines were used to perform Gene chip assay with Affymetrix. The two cell lines, named as S1 and S2 individually, 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.

ORGANISM(S): Mus musculus

SUBMITTER: zuoxiang xiao 

PROVIDER: E-GEOD-65291 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress