Abstract
While immunotherapies for diverse types of cancer are effective in many cases, relapse is still a lingering problem. Like tumor cells, activated immune cells have an anabolic metabolic profile, relying on glycolysis and the increased uptake and synthesis of fatty acids. In contrast, immature antigen-presenting cells, as well as anergic and exhausted T-cells have a catabolic metabolic profile that uses oxidative phosphorylation to provide energy for cellular processes. One goal for enhancing current immunotherapies is to identify metabolic pathways supporting the immune response to tumor antigens. A robust cell expansion and an active modulation via immune checkpoints and cytokine release are required for effective immunity. Lipids, as one of the main components of the cell membrane, are the key regulators of cell signaling and proliferation. Therefore, lipid metabolism reprogramming may impact proliferation and generate dysfunctional immune cells promoting tumor growth. Based on lipid-driven signatures, the discrimination between responsiveness and tolerance to tumor cells will support the development of accurate biomarkers and the identification of potential therapeutic targets. These findings may improve existing immunotherapies and ultimately prevent immune escape in patients for whom existing treatments have failed.
Highlights
Following the discovery of the structure of DNA in 1953 [1], increasingly efficient technologies for the study of the whole genome have enabled assessments of genome-based pathologies in large population cohorts [2]
Immune check points are inhibitory regulators crucial for maintaining self-tolerance and controlling the duration of the immune response in order to prevent collateral tissue damage [13]. Since these key immune-regulatory molecules are used by tumor cells to promote evasion, immune checkpoint inhibitors have demonstrated their effectiveness as clinical targets for cancer immunotherapy [14]
Recent studies propose serum concentrations of very long chain fatty acids (VLCFA) as a way to identify the response to immune checkpoint inhibitors in urological cancer [42]
Summary
Following the discovery of the structure of DNA in 1953 [1], increasingly efficient technologies for the study of the whole genome (genomics) have enabled assessments of genome-based pathologies in large population cohorts [2]. Lipidomics represents an emerging discipline from metabolomics that connects lipid biology, technology and medicine, and that strives to build an all-inclusive atlas of the cellular/tissue lipidome [5] In this regard, the role played by lipids in the etiology and treatment of cancer has loomed large over the last decades. Little work has focused on reviewing context of immune activation in order to explore potential biomarkers and therapeutic targets for how the lipid metabolism is associated with the immune response to tumors. Account, we aim to highlight the role of lipid mediators in the context of immune activation in order to explore potential biomarkers and therapeutic targets for cancer.
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