Lipid Mediators as Therapeutic Targets in Prostate Cancer
- 1Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA 99202, USA
Abstract
Lipid mediators are small molecules, derived from lipid metabolism, that initiate cellular responses. In this review, the major classes of lipid mediators are considered with respect to their effects on prostate cancer cells. These classes are: sphingolipids (sphingosine 1-phosphate and ceramide), glycophospholipids (lysophosphatidic acid; LPA), eicosanoids (prostaglandins, thromboxanes, and leukotrienes), cannabinoids, and free fatty acids. Almost all of these mediators elicit effects by binding to druggable G protein-coupled receptors (GPCRs) to initiate cell proliferation, stimulate migration, and enhance survival. The exceptions are omega-3 fatty acids and endocannabinoids, which inhibit proliferation. The mediators and their receptors serve as potential targets for (1) enzyme inhibitors that block their synthesis, or (2) GPCR antagonists or agonists. These agents are in various stages of development. Progress in testing their translational potential varies between the mediator classes. Lipid mediators also show potential as diagnostic or prognostic biomarkers. Interesting mechanistic aspects have been identified in the course of studying lipid mediator responses in prostate cancer cells. These include positive cross-talk between LPA receptors and EGF receptors, and negative cross-talk between LPA receptors and free fatty acid (FFA) receptors. Together, these findings suggest new strategies for modulating prostate cancer growth and survival pathways in a therapeutic direction.
Related
- The microbiome-metabolome axis in colorectal cancer therapy resistance: mechanisms, mediators, and therapeutic opportunities
- A novel stilbene derivative targets RAD51 activity and sensitizes DU145 prostate cancer cells to cisplatin
- The DNA methylation landscape of prostate cancer is associated with the lipid composition of periprostatic adipose tissue
- Editorial: Lipid signaling in immunity: from inflammation and ageing to cancer and therapeutic opportunities
- The amino acid transporters SLC38A3–SLC38A5–SLC38A7 as novel anti-cancer therapeutic targets
BibTeX
@article{balijepalli2026lipid,
title = {{Lipid Mediators as Therapeutic Targets in Prostate Cancer}},
author = {Pravita Balijepalli and Kathryn E. Meier},
journal = {Cancers},
year = {2026},
month = oct,
doi = {10.3390/cancers18203315},
url = {https://www.mdpi.com/2072-6694/18/20/3315},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Lipid Mediators as Therapeutic Targets in Prostate Cancer
AU - Pravita Balijepalli
AU - Kathryn E. Meier
PY - 2026
DA - 2026/10/14
JO - Cancers
DO - 10.3390/cancers18203315
UR - https://www.mdpi.com/2072-6694/18/20/3315
AB - Lipid mediators are small molecules, derived from lipid metabolism, that initiate cellular responses. In this review, the major classes of lipid mediators are considered with respect to their effects on prostate cancer cells. These classes are: sphingolipids (sphingosine 1-phosphate and ceramide), glycophospholipids (lysophosphatidic acid; LPA), eicosanoids (prostaglandins, thromboxanes, and leukotrienes), cannabinoids, and free fatty acids. Almost all of these mediators elicit effects by binding to druggable G protein-coupled receptors (GPCRs) to initiate cell proliferation, stimulate migration, and enhance survival. The exceptions are omega-3 fatty acids and endocannabinoids, which inhibit proliferation. The mediators and their receptors serve as potential targets for (1) enzyme inhibitors that block their synthesis, or (2) GPCR antagonists or agonists. These agents are in various stages of development. Progress in testing their translational potential varies between the mediator classes. Lipid mediators also show potential as diagnostic or prognostic biomarkers. Interesting mechanistic aspects have been identified in the course of studying lipid mediator responses in prostate cancer cells. These include positive cross-talk between LPA receptors and EGF receptors, and negative cross-talk between LPA receptors and free fatty acid (FFA) receptors. Together, these findings suggest new strategies for modulating prostate cancer growth and survival pathways in a therapeutic direction.
SN - 2072-6694
ER -