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Ferroptosis is a necrotic cell death that is catalyzed by iron ions.
is characterized by the destruction of phospholipid molecules containing long chains of unsaturated fatty acids on the cell membrane after the intracertic reduction system is insulated, causing the cell membrane to rupture.
form of cell death was named Iron Death in 2012.
iron death is closely regulated by intracertic signaling path, iron death is mainly regulated by glutathione peroxidase 4 (GPX4), once GXP4 abnormal, it will lead to cell antioxidant capacity, reactive oxygen accumulation, and ultimately lead to cell iron death.
iron death is associated with Parkinson's disease, pancreatic cancer, diabetes complications, kidney failure, cardiovascular disease and other diseases, and it has been found that iron death can be activated or inhibited to intervene in the development of the disease, so iron death has become a hot research topic in recent years.
cancer cells are known to thrive, divide and reproduce, and therefore have a greater need for metabolism, but this feature also provides clues to their elimination.
the cancer cells to cope with genetic mutations in oxidative stress, making them more resistant to iron death, without which cancer cells can be very sensitive to iron death.
Cancer cells multiply rapidly, which greatly increases the need for metabolism, and the PI3K-AKT-mTOR path is one of the most common mutations in cancer, while the PI3K-AKT-mTOR pathravel mutation is one of the most difficult types of cancer to treat.
recently, a team of professors at memorial Sloan Kettering Cancer Center in the United States published a research paper entitled: Oncogenic activation of PI3K-AKT-mTOR Signaling suppresses fertosis via SREBP-mediated lipesis in the Proceedings of the National Academy of Sciences (PNAS). the
team found that cancer cells often exhibit metabolic changes that make them susceptible to ferroptosis, a particular type of cell death, and found that a combination of drugs that block pi3K-AKT-mTOR and induce iron death can significantly damage and remove tumors.
team found that tumor cells with PY3K-AKT-mTOR pathogenic mutations showed strong resistance to drugs that induce cell iron death in in-body cell experiments.
next, the team will use a combination of drugs that block pi3K-AKT-mTOR access and drugs that induce cell iron death, and the cancer cells will die.
then, the team validated mouse models of breast and prostate cancer with PI3K-AKT-mTOR pathline mutations, and the results showed that the combination of the two drugs could almost completely destroy and remove tumors from mice.
the results, professor Jiang Xuejun, the study's co-author, said it was the most significant tumor retreat ever seen in his lab.
team further demonstrated that the mutated PI3K-AKT-mTOR path path, can increase the activity of proteins involved in cell membrane lipid synthesis, thereby increasing cell membrane lipids and protecting cells from iron death.
the PI3K-AKT-mTOR path, it can pump at the bottom of the kettle, prevent excessive lipid synthesis, and make cells sensitive to iron death.
a paper published in the journal Nature, Jiang Xuejun and others found that certain genetic mutations in the Hippo path pathrapy make cells more sensitive to iron death, providing a new direction for cancer treatment through iron death. the
PNAS study complements and develops the above-mentioned Nature paper, where genetic mutations in many cancers are associated with cell sensitivity to iron death, so that these mutations can be used to start iron death and kill cancer cells, which is expected to be a new and exciting cancer treatment.
it is understood that Professor Jiang's team has applied for a patent related to the study and that the next step will be a combination-of-drug test on tumor samples from cancer patients treated at Memorial Sloan-Kettering Cancer Center.
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