Abstract 1735: Expression of circadian genes correlate with liver metastasis and prognosis in colorectal cancer

Abstract

Abstract The circadian rhythms are daily oscillations in various biological processes, and generated by the feedback loops of eight core circadian genes. These eight genes are, Clock, casein kinase I ε (CKI ε), cryptochrome1 (Cry1) and cryptochrome2 (Cry2), Period1 (Per1), Period2 (Per2) and Period3 (Per3), Bmal1. Recent studies have suggested that the circadian genes participate in the growth and development of various cancers. This study examined the relations of the circadian genes expression to clinicopathological factors and prognosis in patients with colorectal cancer. We studied surgical specimens of cancer tissue and adjacent normal mucosa obtained from 202 patients with untreated colorectal cancer. The relative expression levels of the circadian genes in the specimens were measured by quantitative real-time, reverse-transcription polymerase chain reaction. Expressions of Clock and CKI ε in cancer tissue were significantly higher than those in adjacent normal mucosa. Expressions of Per1 and Per3 in cancer tissue were significantly lower than those in adjacent normal mucosa. Analysis of the relations between clinicopathological features and expressions of the eight circadian genes showed that high expression of the Bmal1 and low expression of the Per1 correlated with liver metastasis. In the analysis of the relations between prognosis and expressions of the eight circadian genes, the prognosis of high expression of the Per2 was significantly better than that of low expression of the Per2. Our results suggest that over-expression of the Bmal1 and reduced expression of the Per1 might promote liver metastasis, and reduced expression of Per2 might shorten prognosis in colorectal cancer. Thus over-expression of the Bmal1 gene and reduced expression of the Per1 gene may be a useful predictor of liver metastasis. And reduced expression of Per2 may be useful as prognostic factor in patients with colorectal cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1735.