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    Home > Active Ingredient News > Antitumor Therapy > elife: The amino acids in the diet determine the fate of cancer cells

    elife: The amino acids in the diet determine the fate of cancer cells

    • Last Update: 2021-05-08
    • Source: Internet
    • Author: User
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    Myc is a powerful oncogene and is associated with most solid tumors, but it is also a powerful driver of cell death.
    Initially, two models were proposed to explain the cell death induced by the Myc gene.
    A "conflict" model believes that the main function of Myc is to induce proliferation, while cells undergo apoptosis in response to abnormal growth signals.
    Another "double" model believes that cell death is a normal and mandatory function of the Myc gene, which is printed on the Myc gene signal transduction itself.
    Myc drives p53-mediated apoptosis through transcriptional regulation of the tumor suppressor ARF.
    In addition to Myc, many other oncogenes are known to induce cell death.

    Src is the first tumor gene to be recognized.
    In human cancers, the expression and activity of Src are often increased, which contributes to the occurrence of tumors.
    Many clinical inhibitors of family kinases (SFKs) targeting Src tumor genes have been developed, but they are not mature enough to be used as therapeutic drugs.

    Drosophila has two SFKs, including Src42A and Src64B.
    Drosophila Src gene regulation has a variety of signaling pathways, including Notch, MAPKs, Jak-Stat, EGF, Wnt and Hippo signaling pathways.
    Src activation can induce cell apoptosis and tissue growth.
    Here, we studied how the Src tumor gene promotes cell proliferation and death in epithelial cells?

    The research team at the Center for Dynamics Research (BDR) found that reducing the consumption of a specific protein can stop cancer cells from growing.
    These findings, published in eLife on April 27, provide the possibility for dietary treatment of cancer.
    Since it is
    known that the carcinogenic process of fruit flies and mammals is the same , this new discovery can help explain the evolution of human cancer.

    It is known that the carcinogenic process of fruit flies and mammals is the same.
    The carcinogenic process of fruit flies and mammals is known to be the same.

    Hiroshi Nishida et al, Methionine restriction breaks obligatory coupling of cell proliferation and death by an oncogene Src in Drosophila, eLife (2021).
    DOI: 10.
    7554/eLife.
    59809

    Hiroshi Nishida et al, Methionine restriction breaks obligatory coupling of cell proliferation and death by an oncogene Src in Drosophila, eLife (2021).
    DOI: 10.
    7554/eLife.
    59809

    Tumors originate from single cells, and when the genes that cause cell proliferation are overactivated, these cells become cancers.
    The activation of a single oncogene in a cell is not enough to make it a cancer cell.
    This phenomenon is considered a "fail-safe" mechanism
    that prevents the cell from easily becoming a cancer.
    For a cell to slip through the gap and become cancer, several other oncogenes and tumor suppressor genes need to be activated in multiple steps.

    The activation of a single oncogene in a cell is not enough to make it a cancer cell.
    This phenomenon is considered to be a "fail-safe" mechanism.
    The
    activation of a single oncogene in a cell is not enough to make it a cancer cell.
    This phenomenon is considered Is a "fail safe" mechanism

    The international research team led by Sa Kan Yoo focused on the tumor gene Src.
    They studied the process of cell proliferation-tumorigenesis-cell death in Drosophila.
    The gene Src independently drives the two processes of cell proliferation and cell death at the same time
    .
    The research team found that the gene p38 is involved in cell proliferation and the gene JNK is involved in cell death.
    The slpr gene activates the genes p38 and JNK at the same time.

    .
    The research team found that the gene p38 is involved in cell proliferation and the gene JNK is involved in cell death.
    The slpr gene activates the genes p38 and JNK at the same time.
    .
    The research team found that the gene p38 is involved in cell proliferation and the gene JNK is involved in cell death.
    The slpr gene activates the genes p38 and JNK at the same time.

    Src activation can induce cell proliferation and death, leading to mild tissue overgrowth

    Src activation can induce cell proliferation and death, leading to mild tissue overgrowth

    "How the oncogene promotes cell death and cell proliferation at the same time has been controversial.
    Our discovery is that the
    oncogene Src promotes cell death and cell proliferation at the same time through a special pathway .
    " Sa Kan Yoo said.

    The oncogene Src promotes cell death and cell proliferation at the same time through a special route.
    The
    oncogene Src promotes cell death and cell proliferation at the same time through a special route.

    The idea of ​​treating cancer can use the "fail-safe" mechanism to inhibit cell proliferation, but not cell death.
    Once researchers determine that activation of p38 is the key to cell proliferation, they can make this concept a research idea, and the activity of gene p38 can be controlled by nutrients in food.
    Therefore, the researchers assessed the relationship with cell proliferation by feeding fruit flies.
    They found that
    reducing the amount of methionine in the diet can control the occurrence of p38 tumors.

    Reducing the amount of methionine in the diet can control the occurrence of p38 tumors.
    Reducing the amount of methionine in the diet can control the occurrence of p38 tumors.

    "We are very excited to find that manipulating the amount of methionine in the diet can affect cell proliferation, but not cell death.
    At present, we don’t know whether these findings in fruit flies can be translated into human cancer treatments.
    Of course, some humans Cancer also activates the gene Src.
    We also found that the slpr gene can mediate the signal pathway controlled by other carcinogens.
    " Sa Kan Yoo added.
    We speculate that
    for tumors with high SFK activity, the treatment of methionine in the diet may have clinical benefits.

    For tumors with high SFK activity, the treatment of methionine in the diet may have clinical benefits.
    For tumors with high SFK activity, the treatment of methionine in the diet may have clinical benefits.

     



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