Recently, American scientists have found a molecule that provides oxygen protection to cells based on the characteristics of lung cells, especially lung cancer cells, which must be present in a high-oxygen environment, and thus developed two new strategies for treating lung cancer. Researchers at the Perlmutter Cancer Center at New York University have found that iron-dependent proteins in lung and breast cancer cells can be destroyed by local release of oxygen molecules, slowing cell growth and making them easier to kill. Related research was published online on November 22nd. NFS1 provides protection against oxygen in cancer cells Human cells contain 48 proteins that depend on a complex of iron and sulfur to function. Iron-sulfur complexes fail when they encounter oxygen molecules. Normal cells must constantly replace these iron-sulfur clusters if they are to survive in a high-oxygen environment such as the lungs. This is especially true if it is abnormally growing lung cancer cells. Current research indicates that lung adenocarcinoma cells that survive under oxygen stress produce more proteins called NFS1, which can extract sulfur from cysteine ​​to make iron-sulfur clusters. The researchers also found that breast cancer cells spread to the lungs and increase NFS1 production to adapt to high oxygen conditions, while the rest of the cells in the breasts do not. Corresponding author Dr. Richard Possemato said: "Our data supports this view: NFS1 provides cancer cells with oxygen protection. We hope to find ways to remove it." NFS1 is not required in hypoxic tissue The team used short hairpin RNA to shut down 2,752 genes involved in cell metabolism, including biochemically related genes for iron and sulfur, and found that many genes essential for survival at high oxygen levels are not so low in a hypoxic environment. important. Strikingly, the NFS1 gene is the most basic in the high-oxygen lungs, but not in cells with much lower oxygen levels. When the researchers injected cancer cells into the skin of mice with and without NFS1, they grew equally well. But the same cells can't form tumors in the lungs without NFS1. Consistent with these findings in mice, human data analysis showed that the level of NFS1 in lung adenocarcinoma cells was significantly higher than in nearby normal lung tissues. Two new ways to stop the growth of lung cancer The authors believe that NFS1 can be critical for the survival of lung cancer cells in two ways. If NFS1 is not active enough to keep up with oxygen-mediated damage to iron-sulfur clusters, the researchers found that cancer cells have problems with important protein construction, but just stop replicating. Alternatively, the number of iron-sulfur clusters can be used as a sensor for iron levels. When the iron level is too low, the cells "believe" that they lack iron and release more from the molecules that store iron. In a study of in vitro culture of cancer cells, the team found that this accumulation of "free" iron causes the production of reactive oxygen species (ROS). This form of damage to the cell membrane and triggering cell death is called ferroptosis. The authors point out that future work needs to prove this effect in living animals. Possemato said: "Our research shows that future anti-cancer treatments - deprivation of cancer cells against ROS antioxidant protection can be combined with drugs that block NFS1, iron-mediated toxicity promotes cancer cell death. Even in hypoxic It can also be performed in tumors." Next, the team will screen for compounds that block NFS1 to promote iron-sulfur cluster production. Shanghai Chuangsai Technology has excellent performance, interleukin cytokines, fetal bovine serum, electrophoresis equipment scientific instruments, raw material drug standards, chemical reagents, cell culture consumables, Shanghai Chuangsai, mass products special promotions, welcome to inquire!
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