| 储小飞,薛晓蕾,赵舒怡,郑啔盛,樊赛军.乙肝病毒X蛋白连接蛋白抑制辐射诱导的乳腺癌细胞自噬调节的研究[J].中华放射医学与防护杂志,2016,36(11):801-805 |
| 乙肝病毒X蛋白连接蛋白抑制辐射诱导的乳腺癌细胞自噬调节的研究 |
| Hepatitis B X-interacting protein (HBXIP) inhibits autophagy induced by ionizing radiation in breast cancer cells |
| 投稿时间：2016-05-13 |
| DOI：10.3760/cma.j.issn.0254-5098.2016.11.001 |
| 中文关键词: 乳腺癌 乙肝病毒X蛋白连接蛋白 STAT3 自噬 |
| 英文关键词:Breast cancer Hepatitis B X-interacting protein STAT3 Autophagy |
| 基金项目:国家自然科学基金（81502664，81402541，81172127）；科技部科研院所技术发展研究专项（2014EG150134）；天津科技支撑计划项目（14ZCZDSY00001） |
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| 中文摘要: |
| 目的 探讨乙肝病毒X蛋白连接蛋白（HBXIP）对电离辐射诱导的乳腺癌细胞自噬的影响。方法 将实验细胞分为对照组、HBXIP转染组、si-HBXIP转染组、HBXIP和si-STAT3共转染组。各处理组给予4 Gy γ射线照射后，0、24、48和72 h采用流式细胞技术检测含嗜酸性自噬体的乳腺癌细胞数；Western blot方法检测LC3-I/II、HBXIP、STAT3蛋白和STAT3（Y705）磷酸化蛋白表达水平的改变。结果 与对照组相比，外源性过表达HBXIP明显减少含有辐射诱导的嗜酸性自噬体的乳腺癌MDA-MB-231细胞数（t24 h=3.67，P<0.05；t48 h=9.74，P<0.01；t72 h=10.15，P<0.01）和自噬相关蛋白LC3-II蛋白的表达；相反，采用siRNA降低HBXIP表达则明显增加含有嗜酸性自噬体的细胞数（t24 h=3.5，P<0.05；t48 h=4.15，P<0.05；t72 h=12.12，P<0.01）和LC3-II的表达。提高HBXIP表达导致剂量依赖性的辐射诱导的STAT3（Y705）磷酸化水平提高；反之，降低HBXIP表达可降低受照细胞中STAT3（Y705）磷酸化水平的表达。采用siRNA-STAT3降低STAT3表达水平，明显降低了HBXIP对辐射诱导的自噬（t24 h=5.57，P<0.05；t48 h=13.65，P<0.01；t72 h=12.47，P<0.01）和LC3-I/II表达调节能力。结论 HBXIP可通过调节p-STAT3（Y705）磷酸化的表达从而调节辐射诱导的乳腺癌细胞自噬。 |
| 英文摘要: |
| Objective To explore the effect of HBXIP on the autophagy induced by ionizing radiation in breast cancer cells. Methods Experiments included control group, HBXIP transfected group, si-HBXIP transfected group, HBXIP and si-STAT3 co-transfected group. Each group was given 4 Gy γ-ray irradiation exposure. Autophagosomes and autolysosomes (AVOs) were quantified by flow cytometry, and the expressions of LC3, HBXIP, STAT3 and STAT3(Y705) phosphorylation proteins were detected by Western blot assay at 0, 24, 48, 72 h post-irradiation. Results Overexpression of HBXIP significantly reduced the increases of AVOs formation(24 h:t=3.67, P<0.05; 48 h:t=9.74, P<0.01; 72 h:t=10.15, P<0.01) and LC3-II protein expression, while si-RNA-mediated depletion of HBXIP expression markedly improved AVOs formation(24 h:t=3.5, P<0.05; 48 h:t=4.15, P<0.05; 72 h:t=12.12, P<0.01) and LC3-II protein expression in irradiated breast cancer cells. In addition, an increased phosphorylation level of STAT3 protein at Y705 in the cells overexpressed HBXIP, and a decreased phosphorylation of STAT3 protein in the cells with silencing HBXIP were observed following irradiation. Meanwhile, STAT3 siRNA inhibited HBXIP functions in regulation of AVOs formation(24 h:t=5.57, P<0.05; 48 h:t=13.65, P<0.01; 72 h:t=12.47, P<0.01) and LC3-II expression in irradiated cells. Conclusions HBXIP inhibits autophagy caused by radiation in breast cancer cells by mediating STAT3 phosphorylation. |
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