Cholesterol Metabolism and Prostate Cancer Dynamics
Summary
Cholesterol is a central lipid molecule that fulfils structural and signalling roles within prostate cells, serving as a precursor for membrane synthesis, androgen biosynthesis and the formation of specialised microdomains known as lipid rafts. Tumour cells commonly reprogramme cholesterol homeostasis by upregulating uptake via low-density lipoprotein (LDL) receptors, enhancing de novo synthesis through the mevalonate pathway and storing excess cholesterol as cholesteryl esters in lipid droplets. These adaptations support rapid proliferation, protect against oxidative stress and fuel persistent androgen receptor signalling, particularly in castration-resistant prostate cancer. Aberrant cholesterol metabolism also intersects with key oncogenic cascades such as PI3K/AKT/mTOR and MAPK, reinforcing survival and metastatic potential. Epidemiological data link elevated circulating cholesterol with aggressive disease, while lipid-lowering strategies, including statins, have shown promise in slowing progression. The tumour microenvironment further influences cholesterol flux through stromal interactions and inflammatory mediators, underscoring the metabolic plasticity that drives prostate cancer dynamics and offering multiple avenues for therapeutic intervention.
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Cholesterol Metabolism and Prostate Cancer Dynamics publication trend
The graph below shows the total number of articles in cholesterol metabolism and prostate cancer dynamics across all publications each year (not limited to Nature Index journals).
Technical terms
Cholesteryl ester: A form of stored cholesterol produced by enzymatic esterification, sequestered in lipid droplets within cells.
Lipid rafts: Ordered membrane microdomains enriched in cholesterol and sphingolipids that organise signalling complexes.
Low-density lipoprotein (LDL): A plasma carrier of cholesterol that delivers lipids to cells via receptor-mediated endocytosis.
Scavenger receptor class B type 1 (SR-B1): A cell-surface receptor that mediates selective uptake of high-density lipoprotein (HDL) cholesterol.
PI3K/AKT/mTOR pathway: A signalling cascade that regulates cell growth, survival and metabolism, frequently hyperactivated in cancer.
References
- Cholesterol Dietary Intake and Tumor Cell Homeostasis Drive Early Epithelial Tumorigenesis: A Potential Modelization of Early Prostate Tumorigenesis. Cancers (2024).
- Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover. Cancer & Metabolism (2022).
- Cholesterol Metabolism and Urinary System Tumors. Biomedicines (2024).
- Prostate Cancer—Focus on Cholesterol. Cancers (2021).
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