Gastroenterology & Hepatology Division, Department of Medicine, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA;
Cancers (Basel). 2010;3(1):285-97. doi: 10.3390/cancers3010285.
Intestinal bacteria can contribute to cell proliferation and cancer development, particularly in chronic infectious diseases in which bacteria and/or bacterial components might interfere with cell function. The number of microbial cells within the gut lumen is estimated to be 100 trillion, which is about 10-times larger than the number of eukaryotic cells in the human body. Because of the complexity of the gut flora, identifying the specific microbial agents related to human diseases remains challenging. Recent studies have demonstrated that the stemness of colon cancer cells is, in part, orchestrated by the microenvironment and is defined by high Wnt activity. In this review article, we will discuss recent progress with respect to intestinal stem cells, cancer stem cells, and the molecular mechanisms of enteric bacteria in the activation of the Wnt pathway. We will also discuss the roles of other pathways, including JAK-STAT, JNK, and Notch, in regulating stem cell niches during bacterial infections using Drosophila models. Insights gained from understanding how host-bacterial interaction during inflammation and cancer may serve as a paradigm for understanding the nature of self-renewal signals.
肠道细菌可以促进细胞增殖和癌症发展，特别是在慢性传染病中，细菌和/或细菌成分可能干扰细胞功能。肠道腔中的微生物细胞数量估计为 100 万亿，大约是人体内真核细胞数量的 10 倍。由于肠道菌群的复杂性，确定与人类疾病相关的特定微生物制剂仍然具有挑战性。最近的研究表明，结肠癌干细胞的干性部分是由微环境协调的，并由高 Wnt 活性定义。在这篇综述文章中，我们将讨论肠道干细胞、癌症干细胞以及肠道细菌在 Wnt 通路激活中的分子机制的最新进展。我们还将讨论在使用果蝇模型进行细菌感染时，其他途径（包括 JAK-STAT、JNK 和 Notch）在调节干细胞龛中的作用。从理解炎症和癌症期间宿主-细菌相互作用中获得的见解可能成为理解自我更新信号本质的范例。
