ArticleJournal of neuro-oncology2009
c-Met-targeted RNA interference inhibits growth and metastasis of glioma U251 cells in vitro.
Article in Journal of neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- The Role of Micro RNAs in Regulating PI3K/AKT Signaling Pathways in Glioblastoma.Iranian journal of pathology · 2022Review
- Anti-neoplastic Effect of Ginkgolide C through Modulating c-Met Phosphorylation in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2020Article
- MicroRNA-562 negatively regulated c-MET/AKT pathway in the growth of glioblastoma cells.OncoTargets and therapy · 2019Article
- Silencing SATB1 overcomes temozolomide resistance by downregulating MGMT expression and upregulating SLC22A18 expression in human glioblastoma cells.Cancer gene therapy · 2018Article
- Alteration status and prognostic value of MET in head and neck squamous cell carcinoma.Journal of Cancer · 2016Article
- Knockdown of c-MET induced apoptosis in ABCB1-overexpressed multidrug-resistance cancer cell lines.Cancer gene therapy · 2015Article
- In vitro and in vivo radiosensitization of human glioma U251 cells induced by upregulated expression of SLC22A18.Cancer gene therapy · 2014Article
- Inhibition of human glioma U251 cells growth in vitro and in vivo by hydroxyapatite nanoparticle-assisted delivery of short hairpin RNAs against SATB1.Molecular biology reports · 2014Article
- Novel siRNA delivery strategy: a new "strand" in CNS translational medicine?Cellular and molecular life sciences : CMLS · 2014Review
- In vitro and in vivo radiosensitization induced by hydroxyapatite nanoparticles.Neuro-oncology · 2013Article
- Predictive value of the SLC22A18 protein expression in glioblastoma patients receiving temozolomide therapy.Journal of translational medicine · 2013Article
- The decreased metastatic potential of rhabdomyosarcoma cells obtained through MET receptor downregulation and the induction of differentiation.Cell death & disease · 2013Article
- Upregulation of SATB1 is associated with the development and progression of glioma.Journal of translational medicine · 2012Article
- Hydroxyapatite nanoparticles inhibit the growth of human glioma cells in vitro and in vivo.International journal of nanomedicine · 2012Article
- Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma.Journal of translational medicine · 2011Article
- Gain of chromosome 7 by chromogenic in situ hybridization (CISH) in chordomas is correlated to c-MET expression.Journal of neuro-oncology · 2011Article
- Cell delivery of Met docking site peptides inhibit angiogenesis and vascular tumor growth.Oncogene · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis plays an essential role in tumor growth and metastasis and is a promising target for cancer therapy. c-Met, a receptor tyrosine kinase, and its ligand, hepatocyte growth factor (HGF), are critical in cellular proliferation, motility, invasion, and angiogenesis. The present study was designed to determine the role of c-Met in growth and metastasis of glioma U251 cells using RNA interference (RNAi) technology in vitro. We constructed three kinds of shRNA expression vectors aiming at the c-Met gene, then transfected them into glioma U251 cells by lipofectamine(TM) 2000. The level of c-Met mRNA was investigated by real-time polymerse chain reaction (RT-PCR). The protein expression of c-Met was observed by immunofluoresence staining and western blotting. U251 cell growth and adherence was detected by methyl thiazole tetrazolium assay. The apoptosis of U251 cells was examined with a flow cytometer. The adherence, invasion, and in vitro angiogenesis assays of U251 cells were done. We got three kinds of c-Met specific shRNA expression vectors which could efficiently inhibit the growth and metastasis of U251 cells and the expression of c-Met in U251 cells. RT-PCR, immunofluoresence staining and western blotting showed that inhibition rate for c-Met expression was up to 90%, 79% and 85%, respectively. The expression of c-Met can be inhibited by RNA interference in U251 cells, which can inhibit the growth and metastasis of U251 cell and induce cell apoptosis. These results indicate that RNAi of c-Met can be an effective antiangiogenic strategy for glioma.
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