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MicroRNA-23a promotes neuroblastoma cell metastasis by targeting CDH1

CDH1 inactivation is important in tumor metastasis. In the present study, it was suggested that the mRNA and protein levels of CDH1 decreased in metastatic neuroblastoma (NB) tissues compared with those in primary NB tissues. The aim of the study was to explore the regulatory mechanisms of CDH1 down...

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Detalles Bibliográficos
Autores principales: CHENG, LIN, YANG, TAO, KUANG, YONGQIN, KONG, BIN, YU, SIXUN, SHU, HAIFENG, ZHOU, HUTIAN, GU, JIANWEN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919791/
https://www.ncbi.nlm.nih.gov/pubmed/24520301
http://dx.doi.org/10.3892/ol.2014.1794
Descripción
Sumario:CDH1 inactivation is important in tumor metastasis. In the present study, it was suggested that the mRNA and protein levels of CDH1 decreased in metastatic neuroblastoma (NB) tissues compared with those in primary NB tissues. The aim of the study was to explore the regulatory mechanisms of CDH1 downregulation in metastatic NB. MicroRNAs are small non-coding RNAs (~22 nt in length) that negatively regulate target mRNAs and are involved in various cancer-related processes, including metastasis. In the current study, miR-23a was shown to be upregulated in human metastatic NB tissues compared with primary NB tissues. Inhibition of miR-23a may significantly suppress NB cell migration and invasion. In vitro reporter assay suggested that CDH1 is a direct target gene of miR-23a. Furthermore, blocking the expression of miR-23a partly restored the expression of CDH1 in NB cells. These findings provide evidence that miR-23a is key in promoting NB cell migration and invasion through targeting CDH1, and suggest that exogenous miR-23a may have therapeutic value in treating NB metastasis.