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Oncogenic transcriptome of A/J lungs
Author(s) -
Gohil Kishorchandra,
Oommen Saji,
Vasu Vihas T,
Cross Carroll E,
Witschi Hanspeter
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.470.2
Subject(s) - biology , carcinogenesis , transcriptome , gene , gene expression , rna , genetics , repressor , cancer research
The specific aim of this study was to identify gene‐networks that may cause lung oncogenesis in a mouse cancer model. A/J mice, in contrast to C57Bl6 (B6) have a high incidence of spontaneous lung tumors. To identify the oncogenic genes, RNA was isolated from lungs of A/J and B6 mice and analyzed with GeneChips for ~14,000 mRNAs. ~2000 differentially expressed genes could be divided in two major classes; overexpressed (~50%) or under expressed in A/J‐lungs compared to those in B6 lungs. Functional clustering identified ~20 distinct clusters, in each major class. These clusters included transcription factors, protein kinases, RNA processors, translation, mitochondrial, and immune response genes. Remarkably, these functional clusters were present in both, over expressed and under‐expressed gene‐classes. But the specific genes within a cluster were unique to each major class. Also noteworthy was the simultaneous over‐expression and under‐expression of protein kinases and, lack of protein phosphatase cluster in overexpressed gene‐class. In addition, a cluster of chromatin‐remodelling genes with repressor activities were differentially expressed between A/J and B6 strains. These transcriptomic analyses identify unique macro‐molecular networks that may contribute to spontaneous oncogenesis and offer targets for anti‐oncogenic interventions, possibly by RNA‐interference.