how does lipid disruption feed inflammation?

Could colorectal cancer be better treated by targeting lipid metabolism? This is the hypothesis of a recent study published in the journal Gutwhich reveals that lipid dysregulation plays a crucial role in the persistence of inflammation, a key factor in the development of this disease.

Persistent inflammation

Colorectal cancer, the third most common cancer worldwide, is a leading cause of cancer-related deaths. Chronic inflammation is recognized as a driver of its progression. Under normal conditions, the body initiates a key process that allows inflammation to resolve naturally. But in colorectal cancer, this process seems to fail, leading to persistent inflammation, we read in a press release.

In this study, researchers analyzed 81 pairs of tumor and healthy tissue samples, and thus mapped key enzymes and genes associated with lipid metabolism. The results show a marked pro-inflammatory lipid signature in tumor tissues. In detail, mediators derived from arachidonic acid (AA), such as leukotrienes and 5-HETE, are increasing, while resolving lipoxins are clearly decreasing.

Towards new therapeutic strategies

Tumor-associated macrophages appear to be the main producers of pro-inflammatory mediators. The study identified overexpression of pro-inflammatory enzymes in cancerous tissues. This imbalance contributes to the persistence of inflammation and promotes tumor progression.

The study highlights that colorectal cancer is characterized by a chronic inflammatory state, maintained by disturbed lipid metabolism. These discoveries could pave the way for targeted therapies aimed at restoring the switching of lipid mediators, and thus rebalancing the inflammatory balance and slowing the progression of cancer.