Molecular targets of colorectal cancer transformation revealed by single-cell sequencing

Ulcerative colitis (UC) is associated with a significant risk of colorectal cancer transformation, which is considered one of its major complications. Prolonged chronic inflammation in the colon mucosa can lead to carcinogenesis due to various factors including dysregulation of cell proliferation and apoptosis, abnormal activation of the immune system, as well as DNA damage and repair abnormalities. Furthermore, the release of inflammatory mediators may directly or indirectly promote the formation and growth of cancer cells. The AOM/DSS mouse model is widely utilized to mimic the process of human colorectal cancer development, including chronic inflammation, carcinogenesis, and tumor progression. The model involves the administration of azoxymethane (AOM), a carcinogenic substance that induces DNA mutations and damage in colonic epithelial cells, leading to the initiation of colorectal cancer. Subsequently, dextran sulfate sodium (DSS), a chemical compound that induces intestinal inflammation, is administered through drinking water. The mice are subjected to cycles of DSS treatment interspersed with recovery periods, during which colitis-associated colorectal tumorigenesis occurs. The assessment typically involves monitoring of colon length, tumor formation, and histopathological examination. The mechanisms underlying colorectal cancer transformation in UC remain incompletely understood. However, research suggests that controlling inflammation, implementing standardized treatment protocols, and regular surveillance through colonoscopy and follow-up are crucial for both prevention and early detection of carcinogenesis. Therefore, further investigations into the mechanisms of colorectal cancer transformation in UC and the development of novel prevention and treatment strategies are essential for improving the prognosis and quality of life of UC patients.