Lack of Period1 accelerates colorectal tumorigeneses in APCmin/+ mice

Clock genes drive the circadian rhythm in each cell, and Period1 (Per1) is one of the core genes in mammals. When the clock genes lose their functions due to deficiency, various behavioral and physiological functions are altered. Although many pathological studies have been conducted on clock genes and cancers, the results could be more consistent. In the present study, we aimed to clarify how the lack of Per1 affects the development and progression of colorectal cancer. We recorded survival days and calculated survival rates, measured the number of polyps, performed histological evaluation, and measured β-catenin expression using ApcMin/+Per1-/- mice. The results showed that loss of Per1 caused variation in the survival rate of mice, increased the number of polyps, and increased β-catenin expression. These results suggest that Per1 plays a role in suppressing the development and progression of colorectal cancer.

时钟基因（clock genes）驱动每一个细胞的昼夜节律，Period1（Per1）是哺乳动物的核心时钟基因之一。当日钟基因因功能缺陷丧失功能时，多种行为与生理功能均会发生改变。尽管学界已围绕时钟基因与癌症开展了大量病理学研究，但现有研究结果的一致性仍欠佳。本研究旨在阐明Per1缺失对结直肠癌发生与进展的影响机制。本研究采用ApcMin/+Per1-/-小鼠模型，记录小鼠存活天数并计算存活率，统计息肉数量，开展组织学评估，并检测β-连环蛋白（β-catenin）的表达水平。结果显示，Per1缺失会导致小鼠存活率出现波动，增加息肉数量，并上调β-连环蛋白的表达水平。上述结果表明，Per1在结直肠癌的发生与进展过程中发挥抑癌作用。