ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013
RNAi-mediated gene silencing of vascular endothelial growth factor-C inhibits tumor lymphangiogenesis and growth of gastric cancer in vivo in mice.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Soluble Vegfr3 gene therapy suppresses multi-organ metastasis in a mouse mammary cancer model.Cancer science · 2020Article
- A Novel Role of VEGFC in Cerebral Ischemia With Lung Injury.Frontiers in neuroscience · 2019Article
- [Changes of lymphatic vessel density in lung adenocarcinoma in situ, minimally invasive adenocarcinoma, and invasive adenocarcinoma and the regulatory factors].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- VEGFC/VEGFR3 axis mediates TGFβ1-induced epithelial-to-mesenchymal transition in non-small cell lung cancer cells.PloS one · 2018Article
- Identification of Gene Expression Differences between Lymphangiogenic and Non-Lymphangiogenic Non-Small Cell Lung Cancer Cell Lines.PloS one · 2016Article
- DNA methylation regulates expression of VEGF-C, and S-adenosylmethionine is effective for VEGF-C methylation and for inhibiting cancer growth.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Article
- STAT3 regulation the expression of VEGF-D in HGC-27 gastric cancer cell.American journal of translational research · 2014Article
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5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of vascular endothelial growth factor-C (VEGF-C) has been implicated as a critical molecular signal in tumor development by promoting intratumoral lymphangiogenesis. The aim of this study was to explore whether small hairpin RNA (shRNA) targeting VEGF-C could inhibit gastric cancer lymphangiogenesis and tumor growth. Plasmid-mediated expression of VEGF-C-shRNA was employed to silence VEGF-C gene expression in human SGC-7901 cell lines. The inhibition of the target gene expression was quantified by real-time quantitative polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay. In vitro, the cell viability was determined by MTT assay, flow cytometry analysis, and migration assay. After VEGF-C knockdown was confirmed, the stable cells were inoculated into nude mice. Tumor growth, lymph vessel density (LVD), and microvascular density were compared for mice administered either VEGF-C-shRNA or control. VEGF-C-shRNA causes effective and specific downregulation of VEGF-C expression (P<0.05). The migration activity of SGC-7901 cells was attenuated in vitro (P<0.05). Tumor growth rate and LVD was suppressed in vivo (P<0.05). VEGF-C-shRNA effectively suppressed gastric cancer cell migration in vivo, retards tumorigenicity, and lymphangiogenesis in nude mice.
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