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    Home > Medical News > Medical World News > Reveals the molecular mechanism of out-of-control camp molecules that induce liver cancer

    Reveals the molecular mechanism of out-of-control camp molecules that induce liver cancer

    • Last Update: 2020-11-09
    • Source: Internet
    • Author: User
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    Since humans first controlled the fire, they have been camping around the fire, spreading information, signaling each other when there is danger, and similarly, specific molecules carrying special information around the cells may be able to help regulate the function of our bodies as needed, and a molecule called ring AMP (cAMP) may move freely within the cell. And to help manage the different processes of the body, and it seems that it seems to be in the right place and at the right time to constantly respond to changes in the environment, so it is not clear to scientists, scientists from the University of California and other institutions to explain this, the results of the study published in the international journal Cell.
    Photo Source: CNBC researcher Professor Susan Taylor said: 'We are very interested in studying the effects of camp on the health of the body, in which we engineered fluorescence tools to combine gene editing technology CRISPR with biosensor technology The fluorescent probe could help researchers look inside cells in a whole new way, and it turns out that out-of-control camp may lead to a rare form of liver cancer, fibroblastular hepatocellular carcinoma (FLC, fibrolamellar carcinoma).
    the researchers explain that cAMP and calcium ions are two important secondary signaling molecules needed by human cells, and their action points are usually carefully regulated by binding proteins, kinases, and stent proteins, which form signaling molecular groups.
    Researchers believe that cells are usually made up of membrane-wrapped cells that function like rooms in a factory, such as the cell's energy factory, mitochondrials, and were surprised to find that a major protein that binds to cAMP can form membraneless (wallless) cells in cells through a process similar to oil droplets forming in water.
    cAMP is dynamically isolated into these membraneless cells, and when these structures are destroyed, cAMP floods cells, causing them to grow out of control, triggering tumors; the researchers say most FLC patients carry a mutation in which important camp-regulating proteins are added to an unrelated protein, although researchers know that the hybrid protein causes FLC tumors to form, but they don't know the exact molecular mechanism.
    In this study, the researchers found that carcinogenic fusion proteins interfere with membraneless cells containing camp, which causes camp to flood cells, while normal liver cells that lose the ability to form membrane-free cells containing camp exhibit out-of-control cell growth patterns, which are a hallmark of cancer, and this study also reveals the specific mechanisms behind the occurrence of FLC and how out-of-control cAMP causes cancer.
    researcher Jin Zhang said that although they account for only 1 percent of the cell's total volume, these membraneless cells absorb 99 percent of the cell tissue, and these membrane-free cells containing CAMP can also be completely interfered with by FLC carcinogenic fusion proteins, which can help researchers accidentally discover the mechanisms of their carcinogenic effects.
    Because camp is important to every human cell and is present in membraneless cells in the brain, heart and pancreatic cells, researchers are currently analyzing the function of these dynamic structures in these particular cell types; In-depth analysis of what else is still in these membraneless cells, and in-depth understanding of what exactly the rules can promote the entry of special molecules and stay in these membraneless cells, because it is directly related to the occurrence of cancer, later researchers will continue to study at the molecular level to reveal the molecular mechanisms of out-of-control camp-induced cancer.
    author of the article, Little Simba Note: The original text has a cut-out reference. Yosuke Chiba; Toshinori Kawanami; Kei Yamasaki; Keigo Uchimura; Atsuji Matsuyama; Kazuhiro Yatera.Hyper-progressive disease after immune checkpoint resor in SMARCA4-deficient small-cell lung carcinoma. (J). Respirology Case Reports.2020. Wang Hui; Mou Shaoyu; Tu Min.Study on the Effect of Nano Albumin Paclitaxel Combined with Carboplatin in the Treatment of Lung Squamous Cell Carcinoma. (J). Journal of nanoscience and nanotechnology.2020. Aya Miyagawa-Hayashino; Satoru Okada; Naoko Takeda-Miyata; Yasutoshi Takashima; Tadaaki Yamada; Yoshizumi Takemura; Junji Uchino; Masayoshi Inoue; Koichi Takayama; Eichi Konishi.TTF-1 and c-MYC-defined Phenotypes of Large Cell Neuroendocrine Carcinoma and Delta-like Protein 3 Expression for Treatment Selection. Applied Immunohistochemistry and Molecular Morphology.2020
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