Data from Overexpression and Hypomethylation of <i>Flap Endonuclease 1</i> Gene in Breast and Other Cancers

Abstract

<div>Abstract<p>Flap endonuclease 1 (FEN1) is a structure-specific nuclease best known for its critical roles in Okazaki fragment maturation, DNA repair, and apoptosis-induced DNA fragmentation. Functional deficiencies in <i>FEN1</i>, in the forms of somatic mutations and polymorphisms, have recently been shown to lead to autoimmunity, chronic inflammation, and predisposition to and progression of cancer. To explore how FEN1 contributes to cancer progression, we examined <i>FEN1</i> expression using 241 matched pairs of cancer and corresponding normal tissues on a gene expression profiling array and validated differential expression by quantitative real-time PCR and immunohistochemistry. Furthermore, we defined the minimum promoter of human <i>FEN1</i> and examined the methylation statuses of the 5′ region of the gene in paired breast cancer tissues. We show that <i>FEN1</i> is significantly up-regulated in multiple cancers and the aberrant expression of <i>FEN1</i> is associated with hypomethylation of the CpG island within the <i>FEN1</i> promoter in tumor cells. The overexpression and promoter hypomethylation of <i>FEN1</i> may serve as biomarkers for monitoring the progression of cancers. (Mol Cancer Res 2008;6(11):1710–7)</p></div>