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SNAIL transcription factor increases the motility and invasive capacity of prostate cancer cells
Indexado
WoS WOS:000367867700022
Scopus SCOPUS_ID:84954270746
DOI 10.3892/MMR.2015.4585
Año 2016
Tipo artículo de investigación

Citas Totales

Autores Afiliación Chile

Instituciones Chile

% Participación
Internacional

Autores
Afiliación Extranjera

Instituciones
Extranjeras


Abstract



The incidence and mortality rates of prostate cancer (PCa) are increasing, and PCa is almost the second-leading cause of cancer-associated mortality in men. During tumor progression, epithelial cells decrease the number of adhesion molecules, change their polarity and position, rearrange their cytoskeleton and increase their migratory and invasive capacities. These changes are known under the concept of epithelial-mesenchymal transition (EMT). EMT is characterized by an upregulation of certain transcription factors, including SNAILl, which represses genes that are characteristic of an epithelial phenotype, including E-cadherin, and indirectly increase the expression levels of genes, which are associated with the mesenchymal phenotype. It has been suggested that the transcription factor, SNAILl, decreases the proliferation and increases the migratory and invasive capacities of PCa cell lines. The present study was performed using LNCaP and PC3 cell lines, in which the expression levels of SNAIL1 were increased or silenced through the use of lentiviral vectors. The expression levels of EMT markers were quantified using reverse transcription-quantitative polymerase chain reaction and western blot analysis. In addition, cell survival was analyzed using an MTS assay; cell proliferation was examined using an antibody targeting Ki-67; migration on plates with 8 mu m pores to allow the passage of cells; and invasiveness was analyzed using a membrane chamber covered in dried basement membrane matrix solution. The levels of apoptosis were determined using a Caspase 3/7 assay containing a substrate modified by caspases 3 and 7. The results demonstrated that the overexpression and silencing of SNAIL1 decreased cell proliferation and survival. However, the overexpression of SNAIL1 decreased apoptosis, compared with cells with the SNAIL1-silenced cells, in which cell apoptosis increased. The migration and invasive capacities increased in the cells overexpressing SNAILl, and decreased when SNAIL1 was silenced. In conclusion, PCa cells overexpressing SNAIL1 exhibited characteristics of an EMT phenotype, whereas the silencing of the SNAIL1 transcriptional repressor promoted an epithelial-like phenotype, with decreased migration and invasion, characteristic of mesenchymal cells.

Revista



Revista ISSN
Molecular Medicine Reports 1791-2997

Métricas Externas



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Disciplinas de Investigación



WOS
Medicine, Research & Experimental
Oncology
Scopus
Sin Disciplinas
SciELO
Sin Disciplinas

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Publicaciones WoS (Ediciones: ISSHP, ISTP, AHCI, SSCI, SCI), Scopus, SciELO Chile.

Colaboración Institucional



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Autores - Afiliación



Ord. Autor Género Institución - País
1 Osorio, Luis A. Hombre Universidad de Chile - Chile
2 FARFAN-TRONCOSO, NANCY MARIA Mujer Universidad de Chile - Chile
3 CASTELLON-VERA, ENRIQUE ALEJANDRO Hombre Universidad de Chile - Chile
4 CONTRERAS-MUNOZ, HECTOR RUBERLY Hombre Universidad de Chile - Chile

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Origen de Citas Identificadas



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Citas identificadas: Las citas provienen de documentos incluidos en la base de datos de DATACIENCIA

Citas Identificadas: 2.7 %
Citas No-identificadas: 97.3 %

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Citas identificadas: Las citas provienen de documentos incluidos en la base de datos de DATACIENCIA

Citas Identificadas: 2.7 %
Citas No-identificadas: 97.3 %

Financiamiento



Fuente
Fondo Nacional de Ciencia y Tecnología

Muestra la fuente de financiamiento declarada en la publicación.

Agradecimientos



Agradecimiento
The authors of the present study would like to thank Ms. Graciela Caroca for her technical assistance. The present study was supported by grants from the Fondo Nacional de Ciencia y Tecnologia [grant nos. 1151214 and 1110269 to Dr Hector R Contreras, and 1140417 to Dr Enrique A Castellon).

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