Nat Med's great discovery! Don't zinc cancer patients at will, may accelerate death!
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Last Update: 2018-06-08
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Source: Internet
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Author: User
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June 8, 2018 / bioin / - patients with metastatic cancer will experience severe deterioration of skeletal muscle quality and function - also known as cachexia Cachexia can lead to poor prognosis and accelerate the death of cancer patients However, researchers know little about the mechanism behind cachexia, which greatly hinders the development of drugs to treat the disease Photo source: cc0 public domain in order to reveal the molecular mechanism behind the disease to help target the development of new drugs, scientists from Columbia University, Northwest University and other units in swarnali Under the leadership of Professor acharyya, it was found that the metal ion transporter Zrt / IRT like protein 14 (ZIP14) is a key factor that mediates cancer-induced cachexia Relevant research results were recently published in nature medicine, entitled "metastatic cancers promote cachexia through ZIP14 upregulation in skeletal muscle" The researchers found that ZIP14 expression increased in skeletal muscles of mice with metastatic cancer and patients with cachexia, while TNF - α and TGF - β induced ZIP14 expression to increase Notably, the researchers found that germ cell stage or muscle specific knockout of ZIP14 significantly reduced muscle atrophy in animal models of metastatic cancer The researchers also found that zinc uptake by ZIP14 mediated muscle precursor cells inhibited MyoD and MEF2C expression and myocyte differentiation More importantly, ZIP14 can mediate zinc enrichment in differentiated muscle cells, thus inducing myosin heavy chain loss These results reveal that zinc homeostasis, which has not been found in the past, plays an important role in muscle atrophy induced by metastatic cancer, indicating that ZIP14 is a key therapeutic target for cachexia Reference: Gang Wang et al, metastatic cancers promote cachexia through ZIP14 upregulation in skeletal muscle, Nature Medicine (2018) Doi: 10.1038/s41591-018-0054-2
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