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    Home > Biochemistry News > Biotechnology News > Calcium-mucoprotein-mediated intercellular interaction regulates the iron death mechanism of cancer cells

    Calcium-mucoprotein-mediated intercellular interaction regulates the iron death mechanism of cancer cells

    • Last Update: 2020-06-08
    • Source: Internet
    • Author: User
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    Glutathione peroxidase 4 (GPX4) is a vital regulator for iron death, which protects cells by moderateing lipid peroxides, of which lipid peroxides are by-products of cellular metabolismIron death can be triggered by direct inhibition of GPX4, or by removing its substrate glutathione or by indirectly inhibiting GPX4 by precursor molecules used to produce glutathione,e.gcysteineiron death helps to enhance the anti-tumor function of several tumor suppressor sprees, such as p53, BAP1 and Yanhuso acidaseHowever, counterintuitively, interstitial cancer cells that are prone to metastasis and often resistant to various treatments are highly sensitive to iron deathimages from Nature, 2019, doi:10.1038/s41586-019-1426-6In a new study, team Zhi-Nan Chen of the Chinese Air Force Military Medical University and the Xuejun Jiang team at memorial Sloan Kettering Cancer Center in the United States found that calcite-based intercellular interactions can regulate iron death non-cell-autonomouslyThe findings were published online July 24, 2019 in the journal Natue under the title "Intercellular perce cation cell ferroptosis via NF2-YAP signalling"in epithelial cells, this interaction mediated by E-calcium mucoprotein inhibits iron death by activating intracellular NF2 (also known as merlin) and Hippo signaling pathwaysInhibiting this signal axis allows the transcription co-activator YAP to promote iron death by raising several iron death regulators, including ACSL4 and TFRCThe findings provide new insights into the mechanisms of observations that cancer cells with interstitial or metastasis characteristics are highly sensitive to iron deathnotably, similar mechanisms regulate iron death in some non-epithelial cellsfinally, given that tumor suppressor gene NF2 inactivation is a common carcinogenic event in mesothelioma, these researchers genetically insinuated the tumor suppressor gene NF2 in syllable in the mouse model of malignant mesothelioma, making cancer cells more sensitive to iron deaththese findings demonstrate the role of intercellular interactions and intracellular NF2-YAP signaling pathways in regulating cell iron death, and also suggest that malignant mutations in NF2-YAP signaling pathways may be able to predict the response of cancer cells to potential iron-induced therapyReference: Jiao Wu et alInter interactioncellular dictates cancer cell ferroptosis via NF2-YAP signallingNature, 2019, doi:10.1038/s41586-019-1426-6 original title: Calcium-mucoprotein-mediated intercellular interaction regulates the iron death mechanism of cancer cells
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