Cancer cells hijack a fatty acid to escape immune attack in liver metastases
Liver metastases are among the most common and deadly forms of cancer spread. Now, researchers at VIB and KU Leuven, with international collaborators, have discovered how cancer cells exploit a fatty acid abundant in the liver to evade destruction by the immune system. By disrupting this process, the researchers restored the cancer-fighting activity of immune cells called neutrophils and reduced…
Liver metastases represent one of the most challenging and lethal forms of cancer spread. Researchers at VIB and KU Leuven have uncovered a mechanism by which cancer cells in the liver exploit a fatty acid to evade the immune system. Specifically, they discovered that metastatic cancer cells attach a fatty acid called palmitate to a protein called laminin-511, stabilizing it through the activity of an enzyme called DHHC17.
This process alters the behavior of neutrophils, immune cells that typically attack and eliminate cancer cells. When exposed to the palmitoylated laminin-511, neutrophils form structures called neutrophil extracellular traps (NETs), which can help tumors survive and grow instead of being eliminated. By reducing the activity of the DHHC17 enzyme, researchers found that metastatic growth was decreased, and neutrophil-dependent antitumor effects were restored.
This finding reveals a new way in which metastatic cancer cells reshape their environment to evade immune destruction. The work, published in the journal Nature Metabolism, suggests that targeting palmitoylation could be a potential strategy for future therapies to restore the immune system's ability to control metastatic disease.
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