miR-506 regulates epithelial mesenchymal transition in breast cancer cell lines

Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the...

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Bibliographic Details
Published in:PloS one 2013-05, Vol.8 (5), p.e64273-e64273
Main Authors: Arora, Himanshu, Qureshi, Rehana, Park, Woong-Yang
Format: Article
Language:English
Subjects:
Analysis
Biology
Breast cancer
Breast Neoplasms - pathology
Cancer
Cell adhesion & migration
Cell Adhesion - physiology
Cell cycle
Cell Line, Tumor
Cell Movement - physiology
Cloning
Development and progression
Epithelial-Mesenchymal Transition - physiology
Female
Gene expression
Genes
Growth factors
Humans
Intermediate filament proteins
Kinases
Mathematics
Medical prognosis
Medicine
Mesenchyme
Metastasis
MicroRNA
MicroRNAs
MicroRNAs - physiology
miRNA
Neoplasm Invasiveness
NF-kappa B - metabolism
NF-κB protein
Prognosis
Promoter Regions, Genetic
Signal transduction
Snail protein
Stem cells
Studies
Survival
Transcription
Transforming growth factors
Tumor cell lines
Tumorigenesis
Vimentin
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Description
Summary:Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the expression of mesenchymal genes such as Vimentin, Snai2, and CD151 in MDA-MB-231 human breast cancer cell line. Moreover, NF-κB bound to the upstream promoter region of miR-506 to suppress transcription. Overexpression of miR-506 inhibited TGFβ-induced EMT and suppressed adhesion, invasion, and migration of MDA-MB-231 cells. From these results, we concluded that miR-506 plays a key role in the process of EMT through posttranslational control of EMT-related genes.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0064273