Posted by Lipid metabolism in cancer cells has garnered increasing attention in recent decades. Cancer cells thrive in hypoxic conditions, nutrient deficiency, and oxidative stress and cannot be separated from alterations in lipid metabolism. Therefore, cancer cells exhibit increased lipid metabolism, lipid uptake, lipogenesis and storage to adapt to a progressively challenging environment, which contribute to their rapid growth. Lipids aid cancer cell activation. Cancer cells absorb lipids with the help of transporter and translocase proteins to obtain energy. Abnormal levels of a series of lipid synthases contribute to the over-accumulation of lipids in the tumor microenvironment (TME). Lipid reprogramming plays an essential role in the TME. Lipids are closely linked to several immune cells and their phenotypic transformation. The reprogramming of tumor lipid metabolism further promotes immunosuppression, which leads to immune escape. This event significantly affects the progression, treatment, recurrence, and metastasis of cancer. Therefore, the present review describes alterations in the lipid metabolism of immune cells in the TME and examines the connection between lipid metabolism and immunotherapy.
Lipids significantly influence tumor metastasis and developments. Novel approaches for the treatment of tumors may be found by focusing on lipid metabolism. A variety of inhibitors and drugs have been developed to target lipid uptake, lipogenesis, fatty acid oxidation and lipid storage. These inhibitors have clear anti-tumor effects, and some of these agents have entered clinical trials.
Cyclodextrins are well-known affinity to lipids. Only methyl CD is mentioned in the paper in the folowing context:
Methyl-β-cyclodextrin (MCD), a cholesterol-depleting agent, has a sensitizing effect on a variety of chemotherapeutic drugs. MCD activates the FasR/FasL pathway via p53 and increases the entry of doxorubicin into the nucleus to promote cell death. MCD combined with adriamycin slowed the growth of tumors in mice. MCD enhanced tamoxifen-induced anticancer effects by causing cell cycle arrest and inducing apoptosis. Exogenous cholesterol supplementation abrogated the combined anticancer effects of tamoxifen and MCD
Wu, Y., Pu, X., Wang, X. et al. Reprogramming of lipid metabolism in the tumor microenvironment: a strategy for tumor immunotherapy. Lipids Health Dis 23, 35 (2024). https://doi.org/10.1186/s12944-024-02024-0