Obesity-Linked Mechanisms in Colorectal Cancer
Summary
Obesity is recognised as a major modifiable risk factor for colorectal cancer, exerting its influence through a constellation of interlinked mechanisms. Excess adiposity drives chronic low-grade inflammation, characterised by elevated pro-inflammatory cytokines and altered adipokine secretion, which in turn promotes DNA damage, cellular proliferation and angiogenesis within the colonic mucosa. Dysregulated insulin and insulin-like growth factor signalling further exacerbate epithelial proliferation and inhibit apoptosis, while obesity-induced alterations in the gut microbiota generate metabolites that can damage the intestinal barrier and modulate immune surveillance. Metabolic reprogramming of both tumour and stromal cells—marked by enhanced glycolysis and lipid metabolism—supports tumour growth and immune evasion. Adipose depots adjacent to the colon, notably epiploic adipose tissue, can act as a local reservoir of tumour-promoting factors. Together, these pathways reveal a complex network linking systemic metabolic disturbance to local microenvironment changes that foster initiation, progression and metastasis of colorectal cancer.
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Obesity-Linked Mechanisms in Colorectal Cancer publication trend
The graph below shows the total number of articles in obesity-linked mechanisms in colorectal cancer across all publications each year (not limited to Nature Index journals).
Technical terms
Adipokines: Hormones and cytokines secreted by adipose tissue that influence inflammation, metabolism and tumour behaviour.
Tumour microenvironment: The local cellular and molecular milieu surrounding cancer cells, including immune cells, stromal cells and extracellular matrix.
Immunosuppressive microenvironment: A tumour milieu in which immune cell function is impaired, allowing cancer cells to evade immune surveillance.
Single-cell RNA sequencing: A technique that profiles gene expression in individual cells, revealing cellular heterogeneity within tissues.
Epiploic adipose tissue (EPAT): Fat deposits attached to the colon that can secrete bioactive molecules promoting local tumour growth.
Metabolic reprogramming: Alterations in cellular energy pathways, such as increased glycolysis or lipid oxidation, that support cancer cell proliferation and survival.
References
- Single-cell transcriptome analysis reveals immunosuppressive landscape in overweight and obese colorectal cancer. Journal of Translational Medicine (2024).
- Immunometabolic Profile Associated with Progressive Damage of the Intestinal Mucosa in Adults Screened for Colorectal Cancer: Association with Diet. International Journal of Molecular Sciences (2023).
- Epiploic Adipose Tissue (EPAT) in Obese Individuals Promotes Colonic Tumorigenesis: A Novel Model for EPAT-Dependent Colorectal Cancer Progression. Cancers (2023).
- Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights. Cancers (2020).
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