ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2011
Silencing of c-Met by RNA interference inhibits the survival, proliferation, and invasion of nasopharyngeal carcinoma cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Lipocalin 2 Reduces MET Levels by Inhibiting MEK/ERK Signaling to Inhibit Nasopharyngeal Carcinoma Cell Migration.Cancers · 2022Article
- LINC00839 knockdown restrains the metastatic behavior of nasopharyngeal carcinoma by sponging miR-454-3p.Aging · 2021Article
- Anti-neoplastic Effect of Ginkgolide C through Modulating c-Met Phosphorylation in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2020Article
- Long Noncoding RNA HOXA11-AS Modulates the Resistance of Nasopharyngeal Carcinoma Cells to Cisplatin via miR-454-3p/c-Met.Molecules and cells · 2020Article
- Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Knockdown of c-MET induced apoptosis in ABCB1-overexpressed multidrug-resistance cancer cell lines.Cancer gene therapy · 2015Article
- MiR-34c suppresses tumor growth and metastasis in nasopharyngeal carcinoma by targeting MET.Cell death & disease · 2015Article
- [Research progress of HGF/MET signaling pathway in EGFR-TKI resistance in non-small cell lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2014Review
- Met degradation by SAIT301, a Met monoclonal antibody, reduces the invasion and migration of nasopharyngeal cancer cells via inhibition of EGR-1 expression.Cell death & disease · 2014Article
- Increased hepatocyte growth factor and c-Met receptor expression in nasopharyngeal carcinoma.International journal of clinical and experimental medicine · 2014Article
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5 authors.
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Abstract
c-Met is a tyrosine kinase receptor that mediates pleiotropic cellular responses following its activation by hepatocyte growth factor. The overexpression of c-Met in nasopharyngeal carcinoma (NPC) has been described recently, but the functional role of c-Met in NPC remains incompletely understood. This study aimed to investigate the potential mechanism by which c-Met contributes to the tumorigenesis of NPC. In the present study, by using RNA interference we silenced the expression of c-Met in CNE-2 cells, a poorly differentiated NPC cell line. Our in vitro studies showed that shRNA-mediated depletion of c-Met resulted in the suppression of proliferation, migration, and invasion, as well as an increase in the apoptosis of CNE-2 cells. Moreover, in xenograft nude mice we demonstrated that the depletion of c-Met resulted in reduced tumor growth and increased apoptosis in xenografts. Taken together, these results suggest that c-Met plays an oncogenic role in the development of NPC and reveal it as a potential novel therapeutic target for NPC.
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