Cell heavy evidence: "God medicine" metformin "anti-cancer mystery" was cracked!
Cell heavy evidence: "God medicine" metformin "anti-cancer mystery" was cracked!
December 22, 2016 Source: Bio Discovery
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];In recent years, there is ample evidence that metformin, a drug widely used to treat type 2 diabetes, can be used to prevent cancer or slow the growth of certain cancers. However, the mechanism behind the anticancer effect of metformin remains unclear.
On December 15th, published in the Cell issue entitled "An Ancient, Unified Mechanism for Metformin Growth Inhibition in C. elegans and Cancer," a team of scientists at the Massachusetts General Hospital identified the prevention of human cancer cell growth with metformin. A key pathway associated with extending the lifespan of nematodes. The researchers said that this means. This genetic pathway plays an important role in a wide range of organisms.
Dr. Alexander Soukas, co-author of the study, said: "We found that metformin affects the transport of molecules in the nucleus. This reduction in transport capacity translates into the ability of metformin to block cancer growth, and, notably, this shift It is also associated with the ability of metformin to extend lifespan. This study provides new insights into the role of metformin in promoting health."
A large number of studies have found that individuals taking metformin have a reduced risk of developing certain cancers and dying from cancer. Currently, clinical trials examining the effects of metformin on breast, prostate and pancreatic cancer are ongoing. Many research groups are working to identify the molecular targets of metformin. In a previous study, Soukas' team observed that in addition to preventing cancer cells from growing, metformin can delay the growth of nematodes.
In this new study, scientists have found that the effect of metformin on cancer depends on two components of a single genetic pathway: 1) the nuclear pore complex, which is related to the entry or exit of the molecule; 2) An enzyme called ACAD10 (acyl-CoA dehydrogenase family member-10). Specifically, metformin exerts an inhibitory effect on mitochondrial activity, thereby reducing cellular energy and limiting the transport of molecules (specifically RagA-RagC GTPase heterodimers) through the nuclear pore. This process inhibits an important cell growth molecule, mTORC1, which causes ACAD10 to activate, slows the growth of nematodes and prolongs lifespan.
In human melanoma and pancreatic cancer cells, the researchers confirmed that the use of the metformin family of drugs induced the expression of ACAD10. Studies have confirmed that limiting nuclear pore transport and up-regulation of ACAD10 are essential for diterpenoids to reduce cancer cell viability and extend nematode lifespan.
Dr. Soukas said: "Our experiments show two very important things: if we force the nucleus to remain open, or if we permanently turn off ACAD10, metformin can no longer block the growth of cancer cells. This indicates that in a particular environment Nuclear pores and ACAD10 may be manipulated to prevent or treat certain cancers."
The researchers said that the important contribution of ACAD10 to the anticancer effect of metformin is an interesting finding. Because previous studies have shown that ACAD10 is also associated with the anti-diabetic effects of drugs. “We are very interested in ACAD10 now. It is clear that how ACAD10 slows cell growth will provide a new basis for finding new targets for cancer treatment. At the same time, we hope to promote healthy aging by manipulating this pathway,†Soukas said.
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