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  • Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation

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    Author(s)
    Zheng, Tingting
    Chen, Keke
    Zhang, Xue
    Feng, Huanhuan
    Shi, Yu
    Liu, Li
    Zhang, Jun
    Chen, Yun
    Griffith University Author(s)
    Zhang, Jun
    Year published
    2020
    Metadata
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    Abstract
    Glioma is the most common malignant brain tumor. Because of its high degree of malignancy, the effect of surgical treatment, radiotherapy, chemotherapy, or immunotherapy is not ideal. TXNDC9 belongs to thioredoxin domain-containing proteins, which is involved in tumor progression. However, no research associated with TXNDC9 has been reported in glioma. In this study, we found that TXNDC9 was upregulated in glioma. Knockdown of TXNDC9 would prevent proliferation and metastasis, induce the apoptosis rate of glioma cells, and promote the expression Cleaved-caspase3, Cleaved-caspase8, Cleaved-caspase9. Meanwhile, knockdown of ...
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    Glioma is the most common malignant brain tumor. Because of its high degree of malignancy, the effect of surgical treatment, radiotherapy, chemotherapy, or immunotherapy is not ideal. TXNDC9 belongs to thioredoxin domain-containing proteins, which is involved in tumor progression. However, no research associated with TXNDC9 has been reported in glioma. In this study, we found that TXNDC9 was upregulated in glioma. Knockdown of TXNDC9 would prevent proliferation and metastasis, induce the apoptosis rate of glioma cells, and promote the expression Cleaved-caspase3, Cleaved-caspase8, Cleaved-caspase9. Meanwhile, knockdown of TXNDC9 induced autophagy by increasing the level of LC3 and Beclin-1. Cell morphology and expression analysis of GFAP, Vimentin, verified that TXNDC9 could regulate glioma cell differentiation. During this program, the expression of p53 changes dramatically. The apoptosis, autophagy, and cell differentiation program were blocked by p53 inhibitor treatment. In conclusion, the silencing of TXNDC9 induces apoptosis and autophagy in glioma and promotes cell differentiation by controlling p53 and may function as a new mechanism in glioma.
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    Journal Title
    Aging
    Volume
    12
    DOI
    https://doi.org/10.18632/aging.103915
    Copyright Statement
    © 2020 Zheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
    Subject
    Biochemistry and Cell Biology
    Physiology
    Oncology and Carcinogenesis
    TXNDC9
    apoptosis
    autophagy
    differentiation
    glioma
    Publication URI
    http://hdl.handle.net/10072/397601
    Collection
    • Journal articles

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