國家衛生研究院 NHRI:Item 3990099045/13324
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    题名: Insulin-like growth factor binding protein 3 promotes radiosensitivity of oral squamous cell carcinoma cells via positive feedback on NF-kappa B/IL-6/ROS signaling
    其它题名: Insulin-like growth factor binding protein 3 promotes radiosensitivity of oral squamous cell carcinoma cells via positive feedback on NF-κ B/IL-6/ROS signaling
    作者: Wang, SH;Chen, YL;Hsiao, JR;Tsai, FY;Jiang, SS;Lee, AYL;Tsai, HJ;Chen, YW
    贡献者: National Institute of Cancer Research
    摘要: Background Ectopic insulin-like growth factor binding protein 3 (IGFBP3) expression has been shown to enhance cell migration and lymph node metastasis of oral squamous cell carcinoma (OSCC) cells. However, OSCC patients with high IGFBP3 expression had improved survival compared with those with low expression. Therefore, we speculated that IGFBP3 expression may play a role in response to conventional OSCC therapies, such as radiotherapy. Methods We used in vitro and in vivo analyses to explore IGFBP3-mediated radiosensitivity. Reactive oxygen species (ROS) detection by flow cytometry was used to confirm IGFBP3-mediated ionizing radiation (IR)-induced apoptosis. Geneset enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were used to analyze the relationship between IGFBP3 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) signaling. Assays involving an NF-kappa B inhibitor, ROS scavenger or interleukin 6 (IL-6) were used to evaluate the NF-kappa B/IL-6/ROS signaling in IGFBP3-mediated radiosensitivity. Results Ectopic IGFBP3 expression enhanced IR-induced cell-killing in vitro. In vivo, IGFBP3 reduced tumor growth and increased apoptotic signals of tumor tissues in immunocompromised mice treated with IR. Combined with IR, ectopic IGFBP3 expression induced mitochondria-dependent apoptosis, which was apparent through mitochondrial destruction and increased ROS production. Ectopic IGFBP3 expression enhanced NK-kappa B activation and downstream cytokine expression. After IR exposure, IGFBP3-induced NF-kappa B activation was inhibited by the ROS scavenger N-acetyl-L-cysteine (NAC). IGFBP3-mediated ROS production was reduced by the NF-kappa B inhibitor BMS-345541, while exogenous IL-6 rescued the NF-kappa B-inhibited, IGFBP3-mediated ROS production. Conclusions Our data demonstrate that IGFBP3, a potential biomarker for radiosensitivity, promotes IR-mediated OSCC cell death by increasing ROS production through NF-kappa B activation and cytokine production.
    日期: 2021-03
    關聯: Journal of Experimental and Clinical Cancer Research. 2021 Mar;40:Article number 95.
    Link to: http://dx.doi.org/10.1186/s13046-021-01898-7
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1756-9966&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000628221500001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85102465845
    显示于类别:[陳雅雯] 期刊論文
    [李岳倫] 期刊論文
    [江士昇] 期刊論文
    [蔡慧珍] 期刊論文

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