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    Home > Active Ingredient News > Antitumor Therapy > Cell Death Dis: CtBP determines fate of ovarian cancer cells by suppressing DRs

    Cell Death Dis: CtBP determines fate of ovarian cancer cells by suppressing DRs

    • Last Update: 2020-05-29
    • Source: Internet
    • Author: User
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    High-level plasma ovary cancer (HGSOC) is a complex heterogeneous disease that accounts for 70% of epithelial ovarian cancer and is still the deadliest gynecological malignanciesThe main treatment spree for HGSOC is a combination of surgical tumor cell reduction and chemotherapyAlthough the disease was initially sensitive to chemotherapy, most HGSOCs gradually mutated in the genome and eventually returned to incurable diseasesTherefore, understanding the genetic and molecular characteristics of HGSOC proliferation can effectively improve its treatment strategyrecent studies have found that the level of expression of CtBP2 (C-end binding protein 2) increased in epithelial ovarian cancer, especially in highly invasive and highly lethal HGSOC subtypes, and that expression of CtBP2 was associated with poor prognosisHowever, whether the occurrence and development of HGSOC depends on CtBP2 or its side-like homologous CtBP1 is still to be studiedin the study, researchers found that CtBP1/2 can inhibit HGSOC's apoptosis process by silent DR4/5The expression of the expression of low CtBP1/2 will raise DR4/5 expression on average and cause spontaneous apoptosis in cells by activating caspase 8DR4/5 activation caused by CtBP1/2 deficiency also increases the sensitivity of HGSOC cells to apoptosis DR4/5 ligand TRAILconsistent with the function of CtBP1/2 as a transcription suppressor, it is able to bind to the promoter region of DR4/5 and inhibit the expression of DR4/5, the potential mechanism may be achieved by collecting it into inhibitory transcription-regulating complexesThe researchers also found that CtBP 1/2 required joint involvement in DR4/5 inhibitionoverall, the study found that CtBP1/2 is an effective inhibitor that affects the expression and activity of DR4/5, suggesting that CtBP may be a potential therapeutic target for HGSOC
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