Up-regulated miR155 Reverses the Epithelial-mesenchymal Transition Induced by EGF and Increases Chemo-sensitivity to Cisplatin in Human Caski Cervical Cancer Cells

The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited...

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Detalles Bibliográficos
Autores principales: Lei, Cui, Wang, Yanlin, Huang, Yurong, Yu, Han, Huang, Yiling, Wu, Liting, Huang, Liming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527539/
https://www.ncbi.nlm.nih.gov/pubmed/23284982
http://dx.doi.org/10.1371/journal.pone.0052310
Descripción
Sumario:The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited cell proliferation and increased the chemo-sensitivity to DDP in human Caski cervical cancer cells. Further, the overexpression of miR155 increased TP53 expression but reduced SMAD2, and CCND1 expression levels. These data suggest that miR155 negatively regulates EGF-induced EMT. We conclude that miR155 does not act as an oncogene but as a tumour suppressor in Caski cells.

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