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B28. LUNG CANCER BIOMARKERS OF RISK - Dysregulation of mRNAs for REST and REST-Interacting Proteins in Tumor Susceptible Mice: Modulatory Effects of Cigarette Smoke. by Gohil, K; Ott, S; Rashidi, V; Hobson, B; Witschi, HP; Cross, CE; Vasu, VT is a scholarly article available to read on EtoBox.

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RE-1 silencing transcription factor (REST), a ∼83 kDa protein, interacts with several proteins that modulate chromatin structure and the expression of multiple genes. REST has been suggested to be a tumor suppressor or an oncogene. Our focus on REST was stimulated by the data from microarray studies. To identify intrinsic tumorigenic gene networks and early transcriptomic predictors of cigarette smoke (CS) induced tumors we compared the lung transcriptomes of tumor susceptible AJ mice with those of tumor resistant B6 mice, breathing either air or CS, and identified ∼1000 differentially expressed transcripts. Functional classification of these transcripts identified a cluster of genes that is implicated in chromatin remodeling and gene expression. A gene-cluster that was over expressed in air breathing, tumor susceptible lungs included genes encoding REST, histone deacetylase (HDAC), methyl-CpG binding protein (MeCP) and TATA-box binding protein (TBP). Previous studies have shown that physical interactions between these proteins affect the expression of a number of REST-dependant genes. Thus, our data suggest a role for this gene cluster in the increased susceptibility of AJ-mice, i

Author

Gohil, K; Ott, S; Rashidi, V; Hobson, B; Witschi, HP; Cross, CE; Vasu, VT

Publisher

American Thoracic Society

Published

2009

Language

EN