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    Home > Food News > Food Articles > Why does drinking green tea fight cancer? Nature Communications "digs" out the molecular mechanism

    Why does drinking green tea fight cancer? Nature Communications "digs" out the molecular mechanism

    • Last Update: 2021-02-23
    • Source: Internet
    • Author: User
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    Original title: Why can drinking green tea fight cancer? Nature Communications "digs" out the molecular mechanism
    green
    , in China, and even the world is a popular beverage. Many studies have found that it has a certain inhibitory effect on a variety of cancers, including breast cancer, lung cancer, prostate cancer and colon cancer. The chemical prevention effect of green tea on tumors is mainly attributed to polyphenols, of which table-free children's tea without EGCG is the most important. EGCG accounts for 50-80% of green tea tea. One cup (240 ml) of green tea contains 200-300 mg of EGCG. The anti-cancer effects of EGCG have been proven in epidemiology, cell culture, animal studies and clinical trials. P53 played an important role in the anti-tumor properties induced by EGCG. p53 is often referred to as the "gene guardian" and is an important tumor suppressor. The p53 mutation is known to be found in more than 50% of human cancers. However, the molecular mechanism of how EGCG interacts with p53 is not clear.
    In a new study published in Nature Communications on February 13, a team led by Professor Chunyu Wang of the
    America
    Renssler Institute of Technology
    Bio
    Science Department found a previously unknown direct interaction between p53 and EGCG and explained how EGCG enhances the anti-cancer activity of p53, thus pointing out new targets for the development of anti-cancer drugs.
    Wang Chunyu, an expert in the study of specific mechanisms of Alzheimer's disease and cancer using the MRI spectrum, describes p53 as the most important protein in human cancer.
    p53 has several well-known anti-cancer functions, including preventing cell growth to allow DNA repair, activating DNA repair, and initiating procedural cell death called apoptosis when DNA damage cannot be repaired. One end of p53 is called the N-end domain (NTD). NTD is a disordered protein that interacts with many proteins and serves as a hub for cell signaling. Therefore, it can play a variety of functions.
    have found that the interaction between EGCG and p53 prevents protein degradation. Typically, when p53 is produced in the body and binds to a protein called MDM2, it mediates the ubibinization and degradation of p53. MDM2 has been found to mutate and amplification in a variety of tumors, and its amplification is closely related to tumor metastasis. MDM2 is independent of ubibinization, and it inhibits transcription by preventing general transcription factors from binding to NTD. The apoptosis effect of EGCG on human cancer cells was related to its interference with P53 ubibination mediated by MDM2. In a recent study, EGCG was identified from a library of 2,295 phytocherics as an inhibitor of p53-MDM2 interactions.
    in the new study, researchers identified the NTD of p53 as the primary EGCG binding bit, which is the MDM2 binding bit, using surface plasma resonance (SPR) and STD-NMR assays. By combining with NTD, EGCG destroys the interaction of p53-MDM2 and inhibits ubibinization of P53 mediated by MDM2, which is the main degradation pathway of p53. These results provide more details on the mechanisms by which EGCG induces apoptosis of cancer cells and the potential efficacy of EGCG in cancer prevention.
    Wang Chunyu said: "EGCG and MDM2 are combined in the same position as the N-end domain of p53, so EGCG and MDM2 compete with each other. When EGCG binds to p53, the protein does not degrade through MDM2, so the level of p53 increases with direct interaction with EGCG, which means that more p53 has anti-cancer function. This is a very important interaction. Link
    paper:
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