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RNA i‐mediated downregulation of oral cancer overexpressed 1 (ORAOV1) inhibits vascular endothelial cell proliferation, migration, invasion, and tube formation
Author(s) -
Zhao Xin,
Liu Dongjuan,
Wang Lili,
Wu Ruiqing,
Zeng Xin,
Dan Hongxia,
Ji Ning,
Jiang Lu,
Zhou Yu,
Chen Qianming
Publication year - 2016
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12371
Subject(s) - downregulation and upregulation , cell growth , cancer research , rna , endothelial stem cell , cell migration , cell , microbiology and biotechnology , chemistry , biology , gene , biochemistry , in vitro
Background Oral squamous cell carcinoma ( OSCC ) is one of the top ten tumors threatening human health. Oral cancer overexpressed 1 ( ORAOV 1) 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 ORAOV 1 in OSCC ‐induced angiogenesis in vitro . Methods EA .hy926 human endothelial cells were co‐cultured with OSCC cells ( HSC ‐3 and SCC ‐25) transfected with ORAOV 1 ‐specific sh RNA to downregulate ORAOV 1 expression, and analyzed for proliferation, migration, invasion, and tube formation by specific assays. Results EA .hy926 endothelial cells co‐cultured with ORAOV 1‐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. Conclusions Our results show, for the first time, that ORAOV 1 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 ORAOV 1 may be a potential therapeutic strategy against OSCC .