Metabolism and Colorectal Cancer

被引:79
|
作者
Sedlak, Joseph C. [1 ,2 ]
Yilmaz, Omer H. [1 ,3 ]
Roper, Jatin [4 ,5 ]
机构
[1] MIT, Dept Biol, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA
[2] Harvard Med Sch, Harvard MIT MD PhD Program, Boston, MA 02115 USA
[3] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA
[4] Duke Univ, Dept Med, Div Gastroenterol, Durham, NC USA
[5] Duke Univ, Dept Pharmacol & Canc Biol, Durham, NC USA
基金
美国国家卫生研究院;
关键词
colorectal cancer; metabolism; diet; microbiome; STEM-CELL FUNCTION; HIGH-FAT-DIET; VITAMIN-D; MOLECULAR-MECHANISMS; CALORIE RESTRICTION; UP-REGULATION; HUMAN COLON; LIFE-SPAN; OBESITY; RISK;
D O I
10.1146/annurev-pathmechdis-031521-041113
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Reprogrammed metabolism is a hallmark of colorectal cancer (CRC). CRC cells are geared toward rapid proliferation, requiring nutrients and the removal of cellular waste in nutrient-poor environments. Intestinal stem cells (ISCs), the primary cell of origin for CRCs, must adapt their metabolism along the adenoma-carcinoma sequence to the unique features of their complex microenvironment that include interactions with intestinal epithelial cells, immune cells, stromal cells, commensal microbes, and dietary components. Emerging evidence implicates modifiable risk factors related to the environment, such as diet, as important in CRC pathogenesis. Here, we focus on describing the metabolism of ISCs, diets that influence CRC initiation, CRC genetics and metabolism, and the tumor microenvironment. The mechanistic links between environmental factors, metabolic adaptations, and the tumor microenvironment in enhancing or supporting CRC tumorigenesis are becoming better understood. Thus, greater knowledge of CRC metabolism holds promise for improved prevention and treatment.
引用
收藏
页码:467 / 492
页数:26
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