Abstract
Dyslipidemia, characterized by metabolic abnormalities, has become an important participant in colorectal cancer (CRC). Dyslipidemia aggravates intestinal inflammation, destroys the protective mucous layer, and disrupts the balance between injury and recovery. On the other hand, antioxidants induced by oxidative stress enhance glycolysis to maintain the acquisition of ATP allowing epithelial cells with damaged genomes to survive. In the repetitive phase of colitis, survival factors enable these epithelial cells to continuously proliferate. The main purpose is to restore and rebuild damaged mucosa, mainly aiming to recover mucosal damage and reconstruct mucosa, but it is also implicated in the occurrence and malignancy of CRC. The metabolic reprogramming of aerobic glycolysis and lipid synthesis enables these transformed epithelial cells to convert raw carbohydrate and amino acid substrates, thereby synthesizing protein and phospholipid biomass. Stearoyl-CoA desaturase, responsible for the fatty acid desaturation, improves the fluidity and permeability of cell membranes, which is one of the key factors affecting metabolic rate. In response to available fat, tumor cells reprogram their metabolism to better plunder energy-rich lipids and rapidly scavenge these lipids through continuous proliferation. However, lipid metabolic disorders inhibit the function of immune-infiltrating cells in the tumor microenvironment through the cross-talk between tumor cells and immunosuppressive stromal cells, thereby providing opportunities for tumor progress. Nonsteroidal anti-inflammatory drugs and lipid-lowering drugs can decrease the formation of aberrant crypt foci, lower the burden of the adenomatous polyp, and reduce the incidence of CRC. This review provides a comprehensive understanding of dyslipidemia on tumorigenesis and tumor progression and a development prospect of lipid disorders on tumor immunity.
Highlights
Colorectal cancer (CRC) remains the third most common type of cancer and the second leading cause of cancer-related death worldwide [1], especially among people who engage in a western pattern diet without appropriate physical exercise [2, 3]
Inflammatory bowel disease is more vulnerable to hyperlipidemia
Long-lasting intake of large amounts of fat can damage the epithelial junctions, alter the distribution of intestinal bacteria flora, and lead to lipopolysaccharide-induced endotoxemia and activation of the inflammatory pathway. It accelerates the injury of the mucosal epithelium and forms a vicious circle. e enhancement of oxidative stress and the turbulence of inflammatory mediators of the microenvironment have a great influence on the occurrence of tumors
Summary
Colorectal cancer (CRC) remains the third most common type of cancer and the second leading cause of cancer-related death worldwide [1], especially among people who engage in a western pattern diet without appropriate physical exercise [2, 3]. In the progress of colorectal cancer, which is significantly different from that of normal mucosal epithelium, cell proliferation and survival require reprogramming metabolism of lipogenesis-related enzymes [9]. Previous studies were zooming in on a certain field of abnormalities of lipid disorder on tumor growth, invasion, and distant metastasis and were not focused on the occurrence of colitis-associated CRC and its progress [10,11,12]. Is paper summarizes and evaluates the existing evidence about dyslipidemia and colitis-associated colorectal tumorigenesis and progress, discusses the influence of dyslipidemia-related conditions on colitis and the resulting tumorigenesis, and analyzes the effects of tumor metabolic reprogramming and the tug-of-war between tumor and infiltrating immune cells in response to high fat, to have a more comprehensive understanding and to provide early intervention measures In view of the fact that dyslipidemia is an important part of obesity and the high prevalence of diseases related to dyslipidemia worldwide, the causal association between dyslipidemia and colitis-associated CRC should be clarified. is paper summarizes and evaluates the existing evidence about dyslipidemia and colitis-associated colorectal tumorigenesis and progress, discusses the influence of dyslipidemia-related conditions on colitis and the resulting tumorigenesis, and analyzes the effects of tumor metabolic reprogramming and the tug-of-war between tumor and infiltrating immune cells in response to high fat, to have a more comprehensive understanding and to provide early intervention measures
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