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Circadian rhythm has been linked to cancer genesis and development, butthe detailed mechanism by which circadian disruption accelerates tumor growthremains unclear. The purpose of this study was to investigate the effect of circadiandisruption on tumor growth and metastasis in male C57BL/6 mice, using an experimentalchronic jet lag model. Lewis lung carcinoma cells were inoculated into both flanksof the mice following 10 days of exposure to experimental chronic jet lag or controlconditions. The effects on tumor growth and lung metastasis were assessed, andthe effect on gene expression was detected using cDNA microarrays and real-timequantitative RT-PCR. Tumors grew faster in the experimental chronic jet lag micecompared to the control mice (P=0.004). Lung metastases were found in 10 out of24 mice in the chronic jet lag group, but only in 3 out of 24 mice in the LD group(P=0.023). Microarray data showed that in both liver and tumors circadian disruptionaltered the expression of genes, including those related to the cell cycle, apoptosis,the immune response and metastasis suppressor genes. The expression of the Ndrg1gene was suppressed by chronic jet lag. We conclude that circadian disruptioncan promote tumor progression and metastasis by affecting the expression of bothtumor-related genes and metastasis suppressor genes.

Experimental chronic jet lag promotes growth and lung metastasis of Lewis lung carcinoma in C57BL/6 mice