Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma.
Proteomics-based identification of VDAC1 as a tumor promoter in cervical carcinoma.
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基于蛋白质组学鉴定 VDAC1 作为宫颈癌的肿瘤启动子
DOI：
10.18632/oncotarget.10562
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发表时间：
2016-08-09
期刊：
影响因子：
--
通讯作者：
Wang H
中科院分区：
文献类型：
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作者：
Zhang C;Ding W;Liu Y;Hu Z;Zhu D;Wang X;Yu L;Wang L;Shen H;Zhang W;Ren C;Li K;Weng D;Deng W;Ma D;Wang H
我们使用氧化同位素编码亲和标签（OxICAT）来研究人乳头瘤病毒（HPV）相关宫颈癌细胞中蛋白质的整体氧化还原状态，以确定基因治疗的潜在靶点。发现电压依赖性阴离子通道1（VDAC1）在HPV阳性宫颈癌细胞中高度氧化。VDAC1的表达与宫颈癌的侵袭、宫颈上皮内瘤变（CIN）的分级以及CIN中HPV16 E7的表达显著相关。在细胞系中敲低VDAC1会增加细胞凋亡率，而VDAC1的过表达（分别地）则部分逆转了这种效应。因此，VDAC1可能促进HPV相关疾病的恶性进展，而旨在抑制VDAC1的治疗可能预防HPV诱导的宫颈疾病的进展。
We used oxidative isotope-coded affinity tags (OxICAT) to investigate the global redox status of proteins in human papillomavirus (HPV)-related cervical cancer cells, in order to identify a potential target for gene therapy. Voltage-dependent anion channel 1 (VDAC1) was found to be highly oxidized in HPV-positive cervical cancer cells. VDAC1 expression correlated significantly with the invasion of cervical cancer, the grade of cervical intraepithelial neoplasia (CIN) and the expression of HPV16 E7 in CIN. Knockdown of VDAC1 in cell lines increased the rate of apoptosis, while overexpression of the VDAC1 (respectively) partly reversed the effect. Thus, VDAC1 may promote the malignant progression of HPV-related disease, and treatments designed to suppress VDAC1 could prevent the progression of HPV-induced cervical disease.