Immune cells store lipids to help breast cancer cells grow their lungs

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, growth and development. Newly transferred tumor cells to the lungs face a number of survival pressures, such as how to escape the pursuit of immune cells and how to capture energy in unfamiliar environments to survive.
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 the transferred tumor cells from being killed. Little is known about the problem of energy intake of tumor cells, so how do tumor cells that travel thousands of miles to the lungs solve the problem of eating?
, September 21, 2020, Nature Immunology magazine published online a paper entitled "Lung mesenchymal cells elicit lip lip storage in neutrophils that fuel breast cancer lung 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. The study suggests that tumor cells, before metastasis, induce neutral granulocytes to soak in the lungs and store large amounts of lipids, which can be used as a reserve of "grain and grass" by tumor cells once they are transferred to the lungs to promote their implantation and growth.
study, the authors used a mouse breast cancer model to find that from the pre-transfer stage, neutral granulocytes from bone marrow sources accumulate a large amount of lipids after they are immersed in the lungs. This lipid is not inherent in neutral granulocytes, but is induced by CD140a plus interstitial cells when it reaches the lungs.
molecular mechanism, 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-out atgl enhances lipid build-up in cells and significantly promotes lung metastasis in breast cancer in the body. In contrast, 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 derived from neutral granulocytes through cyto-lysosomes, resulting in higher proliferation capacity, and finally, in mouse breast cancer metastasis models, lipid transport (cytophagy) inhibitors can significantly inhibit tumor metastasis. The study reported that pre-metastasis of immune cells (neutrinoblasts) in the micro-environment could serve as a source of energy supply for tumor cells, providing new targets for clinical interventions in breast cancer pulmonary metastasis. (Source: Science Network)
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