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    Home > Biochemistry News > Biotechnology News > Protein imbalances can cause cancer, revealing the non-genetic mechanisms of cancer.

    Protein imbalances can cause cancer, revealing the non-genetic mechanisms of cancer.

    • Last Update: 2020-08-06
    • Source: Internet
    • Author: User
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    Genetic malformations have long been thought to be the leading cause of cancer, but a new study has found that protein imbalances within cells can cause cancer.
    scientists say it is a major breakthrough that reveals the non-genetic mechanisms of cancer.
    published in Oncogene, the study describes protein disorders as a powerful cancer prediction tool to determine whether a patient is responding to chemotherapy or if the tumor has spread to other parts.
    the results open the door to new cancer therapies that target measurements and prevent cellular imbalances.
    imbalance between the two proteins causes cancer Under normal circumstances, cells receive external signals through cell wall binding receptors (FGFR2). After
    stimulation, the receptor is opened within the cell, thus initiating the signaling protein and protein kinase pathways to achieve cell proliferation.
    in some cancer cells, the pathway is permanently opened.
    traditional cancer diagnosis is to look for genetically modified receptors that keep the cell protein pathway open.
    a team led by the University of Leeds and the University of Texas MD Anderson Cancer Center focused on the "AKt Signaling Pathway", a intracellular signaling pathway that drives cancer formation and tumor transmission in the body.
    the researchers observed changes in cancer cells without external stimulation, and found that the "AKt signaling pathway" could also be activated without genetic modification.
    the two proteins, Plcy1 and Grb2, compete for binding to the FGFR2 receptor, and the relative concentration of the protein determines which protein ultimately wins the competition.
    study found that when Plcy1 content is high, the AKt signal path is triggered.
    this way, the imbalance between the two proteins can lead to the proliferation of cancer cells and the formation of tumors. Dr. Zahra Timsah, the lead researcher on the study
    , said the competitive effects of different protein-receptor bindings can cause cancer unexpectedly.
    study also found that when the Grb2 protein in the cell runs out, the FGFR2 receptor is more likely to bind to Plcy1, which causes the cancer to spread uncontrollably.
    But when the content of Grb2 is increased, this uncontrolled situation is reversed and the normal activity of FGFR2 is restored.
    researchers believe that under normal circumstances, the fair play of the two proteins and the normal Plcy1-receptor binding are useful for cells, but when the protein is out of balance, it can cause Plcy1 to lose control, further leading to tumor formation.
    researchers also found that the loss of Grb2 led to the development of multiple tumors near the main tumor, suggesting that the imbalance of the protein played a role in the tumor diffusion process.
    this phenomenon makes sense because Plcy1 plays a role in cell movement.
    researchers used the imbalance between GRb2 and Plcy1 to predict breast cancer and found that higher levels of Grb2 meant a better prognosis and longer survival.
    single-gene screening is not enough - non-genetic factors or understanding of cancer, said Professor John Ladbury, dean of the School of Biological Sciences at the University of Leeds, that sequencing of the human genome has become a huge investment and that the idea has been that if we know all the genetic information, we can predict the risk of cancer and end up treating it with treatmentbased on precision medicine.
    but our research shows that single-gene screening is not enough.
    previous studies have highlighted the root cause of cancer as genetic mutations.
    some studies have pointed out that cancer is not affected by genetic factors, for example, by the epigenetic modification of proteins.
    But the study shows that receptors can also transmit signals when they are not activated, so non-genetic factors may be key to understanding cancer.
    the team is currently working with clinicians at the University of Leeds to study the non-genetic mechanisms of other cancers.
    they are exploring whether other cell receptors, like FGFR2, can produce tumor signals without activation.
    Source: Decoding Medicine.
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