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    Home > Biochemistry News > Biotechnology News > Knocking out the autophagy gene Rb1cc1 is expected to improve the efficacy of PD-1 antibodies, new research suggests

    Knocking out the autophagy gene Rb1cc1 is expected to improve the efficacy of PD-1 antibodies, new research suggests

    • Last Update: 2021-01-12
    • Source: Internet
    • Author: User
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    Autophagy is the process by which cell fragments are reused to create new ingredients, and this waste treatment system is important for the survival of normal cells.
    study, Regeneron researchers found that autophagy can also protect tumor cells from the immune system.
    they used CRISPR screening techniques to identify an autophagy-related gene, Rb1cc1, which makes tumor cells more susceptible to T-cell killing and improves the effectiveness of immunosupger inhibitors in mice.
    results were published in Science Journal on December 18.
    to determine which genes regulate tumor sensitivity to T-cell killing, the researchers screened whole genome CRISPR/Cas9 in colon gland cancer cells in mice.
    they found that the apoptosis signaling induced by the inflammatory molecule TNF-α is a key signaling path for T cells to kill tumor cells.
    : A further study by Science Immunology found that the autophagy process of tumor cells appears to protect them from T-cell death.
    researchers knocked out three key autophagy genes, Rb1cc1, Atg9a and Atg12, and found that tumor cells became sensitive to T-cell killing.
    And in the presence of TNF-α blocking antibodies, knocking out Rb1cc1, Atg9a, or Atg12 has a very limited lethal effect on cancer cells, indicating that the protective effect of autophagy is mainly mediated by the TNF-α path.
    the knock-out of Rb1cc1, Atg9a, or Atg12 also significantly increased TNF-α-induced cell death.
    in a mouse model of breast cancer, the researchers tested whether autophagy infestion increased tumor response to immunosuppressants.
    results showed that knocking out RB1cc1 in mice led to an increase in tumor cell death.
    also observed that tumors that knocked out RB1cc1 in mice completely subsided after being used in association with PD-1 and CTLA-4 antibodies, and that the tumors in the control group were only moderately inhibited by growth.
    similar results were observed in mouse models of colon cancer.
    In tumors that knock out the RB1cc1 gene, knocking out TNF-α subjects at the same time limits the tumor's sensitivity to immunotherapy, suggesting that TNF-α and autophagy are key factors in T-cells killing cancer cells.
    , the study sheds light on the new role of autophagy in cancer, providing the possibility of using autophagy inhibitors to improve the efficacy of immunotherapy drugs in more patients.
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