RNAi‐mediated downregulation of oral cancer overexpressed 1 (ORAOV1) inhibits vascular endothelial cell proliferation, migration, invasion, and tube formation
RNAi‐mediated downregulation of oral cancer overexpressed 1 (ORAOV1) inhibits vascular endothelial cell proliferation, migration, invasion, and tube formation
复制标题
RNAi 介导的口腔癌过表达 1 (ORAOV1) 下调抑制血管内皮细胞增殖、迁移、侵袭和管形成
DOI：
10.1111/jop.12371
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Qianming Chen
中科院分区：
文献类型：
--
作者：
Xin Zhao;Dongjuan Liu;Lili Wang;Ruiqing Wu;Xin Zeng;Hongxia Dan;Ning Ji;Lu Jiang;Yu Zhou;Qianming Chen
口腔鳞状细胞癌（oral squamous cell carcinoma，OSCC）是威胁人类健康的十大肿瘤之一。口腔癌过表达基因1（oral cancer overexpressed 1，ORAOV 1）是口腔鳞癌染色体11 q13区域中最常见的扩增区域之一，被认为是一个新的候选癌基因，在口腔鳞癌中起着调控细胞周期、细胞凋亡和血管生成的作用。本研究通过体外培养人口腔鳞癌细胞和EA.hy926人内皮细胞，观察口腔鳞癌细胞中ORAOV 1的表达情况，探讨ORAOV 1在OSCC诱导血管生成中的作用（HSC-3和SCC-25）转染ORAOV 1特异性shRNA以下调ORAOV 1表达，并分析增殖、迁移、侵袭，结果EA.hy926内皮细胞与ORAOV 1缺陷型口腔鳞癌细胞共培养后，其增殖能力明显降低，迁移，和入侵，以及在管形成的活动相比，在control cells.ConclusionsOur结果表明，第一次，OSCC细胞表达的ORAOV 1促进管形成的内皮细胞，表明其参与OSCC血管生成。考虑到新生血管在肿瘤发展和转移中的重要性，这些发现表明靶向ORAOV 1可能是一种潜在的治疗策略。
BackgroundOral squamous cell carcinoma (OSCC) is one of the top ten tumors threatening human health. Oral cancer overexpressed 1 (ORAOV1) identified within chromosomal region 11q13, one of the most frequently amplified regions in OSCC, has been suggested as a novel candidate oncogene in OSCC, regulating cell cycle, apoptosis, and angiogenesis. In this study, we investigated the role of ORAOV1 in OSCC‐induced angiogenesisin vitro.MethodsEA.hy926 human endothelial cells were co‐cultured with OSCC cells (HSC‐3 and SCC‐25) transfected withORAOV1‐specific shRNA to downregulate ORAOV1 expression, and analyzed for proliferation, migration, invasion, and tube formation by specific assays.ResultsEA.hy926 endothelial cells co‐cultured with ORAOV1‐deficient OSCC cells exhibited significantly lower proliferation, migration, and invasion, as well as the activity in tube formation compared to that in the control cells.ConclusionsOur results show, for the first time, that ORAOV1 expressed by OSCC cells promotes tube formation by endothelial cells, indicating its involvement in OSCC angiogenesis. Considering the importance of neovascularization in tumor development and metastasis, these findings suggest that targeting ORAOV1 may be a potential therapeutic strategy against OSCC.