期刊
CANCERS
卷 13, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cancers13081749
关键词
colon; fibroblasts; stroma; colorectal cancer; inflammation; intestinal stem cells
类别
资金
- Plan Cancer System biology 2017
- region Occitanie
- Universite de Toulouse III
- HoliFAB project - European Union's Horizon 2020 research and innovation program [760927]
- H2020 Societal Challenges Programme [760927] Funding Source: H2020 Societal Challenges Programme
Colorectal cancer (CRC) is the third most common cause of cancer-related death. Patients with inflammatory bowel disease have an increased risk of CRC. The interactions between fibroblasts and ISCs in the colon may play a crucial role in the initiation of CRC due to chronic inflammation. Despite improvements in CRC treatment, including better detection and drug strategies, CRC remains a public health concern.
Simple Summary Colorectal cancer (CRC) is the third most common cause of cancer-related death. Patients suffering inflammatory bowel disease have an increased risk of CRC. It is admitted that CRC found its origin within crypts of the colon mucosa, which host the intestinal stem cells (ISCs) responsible of the tissue renewal. ISC behavior is controlled by the fibroblasts that surround the crypt. During inflammation, the signals delivered by fibroblasts are altered, leading to stem cells' dysregulation, possibly turning them into cancer-initiating cells. Here, we reviewed the interplays between the fibroblast and the ISCs, possibly leading to the initiation of CRC due to chronic inflammation. Colorectal cancer (CRC) is the third most common cause of cancer-related death. Significant improvements in CRC treatment have been made for the last 20 years, on one hand thanks to a better detection, allowing surgical resection of the incriminated area, and on the other hand, thanks to a better knowledge of CRC's development allowing the improvement of drug strategies. Despite this crucial progress, CRC remains a public health issue. The current model for CRC initiation and progression is based on accumulation of sequential known genetic mutations in the colon epithelial cells' genome leading to a loss of control over proliferation and survival. However, increasing evidence reveals that CRC initiation is more complex. Indeed, chronic inflammatory contexts, such as inflammatory bowel diseases, have been shown to increase the risk for CRC development in mice and humans. In this manuscript, we review whether colon fibroblasts can go from the main regulators of the ISC homeostasis, regulating not only the renewal process but also the epithelial cells' differentiation occurring along the colon crypt, to the main player in the initiation of the colorectal cancer process due to chronic inflammation.
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