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    Home > Active Ingredient News > Antitumor Therapy > Cell Death Dis: A New Mechanism for Colorectal Cancer Metastay

    Cell Death Dis: A New Mechanism for Colorectal Cancer Metastay

    • Last Update: 2020-05-29
    • Source: Internet
    • Author: User
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    Colorectal cancer (CRC) is the third most commonly diagnosed malignant tumor and the third highest cancer mortality rate worldwideTumor metastasis is the leading cause of death in patients at the end of CRCThe median survival time in most metastatic CRC patients was only 2 years, and the results were far from satisfactoryRecent studies have found that the tumor microenvironment (TME) is a dynamic and ever-changing network whose interactions with tumor cells are critical to tumor metastasisCAF (cancer-related fibroblasts) is one of the main components of the matrix cells around cancer cells, and the metabolic interaction sympathise with CRC cells plays an important role in the development of CRCHowever, it is not clear how these metabolic reprogramming affects the transfer of CRC cellsin the study,, researchers found that CAFs conditionmedia can facilitate the migration of CRC cells compared to normal fibroblast condition media (CM)CAF was reprogrammed by lipid groups and accumulated more fatty acids and phospholipidsThe study found that CAFs conditional media that removed proteins can still promote the migration of CRC cells, which indicates that small molecular metabolites in CAFs condition mediums are the cause of increased CRC cell migrationresearchers further clarified that CRC cells absorb lipid metabolites secreted by CAF cellsFASN (fatty acid hetine) is the key enzyme in fatty acid synthesis, and its expression level increases significantly in CAFThe expression of CAF-induced CRC cell migration can be effectively inhibited by the expression of siRNA knocking down FASN or by reducing the intake of FATTy acids by using exogenous sulfonyl N-amber amide amine acid or endogenous CD36 monoclonal antibodies, the results of the study illustrate a new metastatic mechanism for colorectal cancer, suggesting that the FASN gene in cancer-related fibroblasts and the CD36 gene in colorectal cancer cells may be potential targets for cancer anti-metastatic treatment
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