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re-expression of DIrAS3 and P53 induces apoptosis and impaired autophagy in head and neck squamous cell carcinoma

Military Medical research 2021年第2期8卷 148-161页

作者： Zhe Liu douglas r.hurst Xing Qu Li-Guang Lu Chen-Zhou Wu Yu-Yu Li Yi Li State Key Laboratory of Oral Diseases&National Clinical research Center for Oral Diseases West China Hospital of StomatologySichuan UniversityChengdu 610041China Department of Head and Neck Oncology West China Hospital of StomatologySichuan UniversityChengdu 610041China Department of Pathology University of Alabama at BirminghamBirminghamAL 35216USA Department of Evidence Based Stomatology West China Hospital of StomatologySichuan UniversityChengdu 610041China.

Background:p53 and DIrAS3 are tumor suppressors that are frequently silenced in *** this study,we sought to determine whether the concurrent re-expression of p53 and DIrAS3 could effectively induce head and neck squamous cell carcinoma(HNSCC)cell ***:CAL-27 and SCC-25 cells were treated with Ad-DIrAS3 and rAd-p53 to induce re-expression of DIrAS3 and p53 *** effects of DIrAS3 and p53 re-expression on the growth and apoptosis of HNSCC cells were examined by TUNEL assay,flow cytometric analysis and *** effects of DIrAS3 and p53 re-expression on Akt phosphorylation,oncogene expression,and the interaction of 4 E-BP1 with eIF4 E were determined by real-time PCr,Western blotting and immunoprecipitation *** ability of DIrAS3 and p53 re-expression to induce autophagy was evaluated by transmission electron microscopy,LC3 fluorescence microscopy and Western *** effects of DIrAS3 and p53 re-expression on HNSCC growth were evaluated by using an orthotopic xenograft mouse ***:TUNEL assay and flow cytometric analysis showed that the concurrent re-expression of DIrAS3 and p53 significantly induced apoptosis(Pric analysis revealed that DIrAS3 and p53 reexpression significantly inhibited proliferation and induced cell cycle arrest(Prrent re-expression of DIrAS3 and p53 down-regulated signal transducer and activation of transcription 3(STAT3)and upregulated p21WAF1/CIP1 and Bax(PrAS3 and p53 re-expression also inhibited Akt phosphorylation,increased the interaction of eIF4 E with 4 E-BP1,and reduced the expression of c-Myc,cyclin D1,vascular endothelial growth factor(VEGF),fibroblast growth factor(FGF),epidermal growth factor receptor(EGFr)and Bcl-2(Preover,the concurrent re-expression of DIrAS3 and p53 increased the percentage of cells with GFP-LC3 puncta compared with that in cells treated with control adenovirus(50.00%±4.55%vs.4.67%±1.25%,P<

关键词： DIrAS3 p53 Apoptosis Autophagy Head and neck squamous cell carcinoma

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转移抑制与metastamir调节的联系

引用

中国肺癌杂志 2010年第2期13卷 140-143页

作者： Mick D.EDMONDS douglas r.hurst Danny r. WELCH 王伟强(翻译) 李书军(翻译) 丁燕(校对) 南娟(校对) Department of Pathology Cancer research-Center for Metastasis research University of Alabama at Birmingham Birmingham AL USA Cell Biology Cancer research-Center for Metastasis research University of Alabama at Birmingham Birmingham AL USA pharmacology/Toxicology Cancer research-Center for Metastasis research University of Alabama at Birmingham Birmingham AL USA Comprehensive Cancer Center Cancer research-Center for Metastasis research University of Alabama at Birmingham Birmingham AL USA National Foundation for Cancer research-Center for Metastasis research University of Alabama at Birmingham Birmingham AL USA 天津医科大学总医院天津市肺癌研究所天津市肺癌转移与肿瘤微环境重点实验室

BrMS1:乳腺癌转移抑制因子1;HDAC:组蛋白去乙酰化酶;EGFr:表皮生长因子受体;mirNA:小分子rNA;mir:小分子rNA;pri-mirNA:初始小分子rNA;

关键词：转移抑制小分子rNA BrMS1 metastamir

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