Nature Immunology: Proactively, cancer cells induce immune cells to store lipids in advance to help them metastasy their lungs.

Metastasis is the leading cause of death from tumor disease, and lung is one of the most common metastasis organs of solid tumors.
for tumor cells, it is necessary to overcome a lot of resistance in order to successfully establish a foothold in the lungs, grow and develop.
newly transferred tumor cells to the lungs face many survival pressures, such as how to escape the immune cells and how to survive by ingesting energy in unfamiliar environments.
It is generally believed that tumor tissue transforms the lung environment before it is transferred to the lungs, weakening the activity of killer T-cells and natural killer (NK) cells, creating an immunosuppressive micro-environment that protects transferred tumor cells from being killed.
little is known about the problem of energy intake of tumor cells, how do tumor cells that travel thousands of miles to the lungs solve the problem of eating? On September 21, 2020, the Jackson Laboratory's Ren Guangwen Task Force published a research paper entitled: Lung mesenchymal cells elicit lipid storage in neutrophils that fuel breast cancer cancer metastasis online.
The study suggests that tumor cells induce neutral granulocytes to soak in the lungs and store large amounts of lipids, which can be used as a reserve of "grain grass" to promote the planting and growth of tumor cells once they are transferred to the lungs.
study, the authors used a mouse breast cancer model to find that from the pre-transfer stage, the bone marrow-sourced neutral granulocytes accumulated a large amount of lipids after being immersed in the lungs.
the lipids are not inherent in neutral granulocytes, but are induced by CD140a plus interstitial cells when they reach the lungs.
molecular mechanisms, interpulmonary charged cells significantly increased the expression of neutral granulocyte lipid drop-related genes, including Hilpda, Cidec, and G0s2.
these upwardly increased triglycerase (ATGL) inhibitors in turn inhibit the enzyme activity of ATGL, leading to the accumulation of triglycerides in the neutral granulocytes of the lungs.
neutral granulocyte-specific knock-off atgl enhances lipid build-up in cells and significantly promotes lung metastasis in breast cancer in the body.
, knocking out the Hilpda gene in neutral granulocytes reduced lipid storage and significantly inhibited metastasis of breast tumors.
further in vitro and in vivo experiments have shown that tumor cells devour lipid-rich vesicles from neutral granulocytes through cell-lysosomes, resulting in higher proliferation capacity.
, in mouse breast cancer metastasis models, inhibitors of lipid transport (cellulation) significantly inhibited tumor metastasis.
the study reported on the new function of pre-metastasis micro-environment immune cells (neutrinoblasts) as a source of energy supply for tumor cells, providing new targets for clinical interventions in breast cancer pulmonary metastasis.
Li Peishan (now an associate professor at Shandong University's School of Basic Medicine) and Lu Ming (now an associate researcher at Huashan Hospital affiliated with Fudan University) are co-authors of the paper, and Ren Guangwen is the author of the paper's newsletter.
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