Next Article in Journal
Gelam Honey Has a Protective Effect against Lipopolysaccharide (LPS)-Induced Organ Failure
Next Article in Special Issue
CD146 Expression Correlates with Epithelial-Mesenchymal Transition Markers and a Poor Prognosis in Gastric Cancer
Previous Article in Journal
Investigation of Antigen-Antibody Interactions of Sulfonamides with a Monoclonal Antibody in a Fluorescence Polarization Immunoassay Using 3D-QSAR Models
Previous Article in Special Issue
Characterization of ARF-BP1/HUWE1 Interactions with CTCF, MYC, ARF and p53 in MYC-Driven B Cell Neoplasms
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2012, 13(5), 6352-6369; doi:10.3390/ijms13056352

Revealing the Anti-Tumor Effect of Artificial miRNA p-27-5p on Human Breast Carcinoma Cell Line T-47D

Department of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan
Institute of Biomedical Informatics, Center for Systems and Synthetic Biology, National Yang-Ming University, Taipei 112, Taiwan
Institute of Information Science, Research Center for Information Technology Innovation, Academia Sinica, Taipei 115, Taiwan
Biodiversity Research Center and Genomics Research Center, Academia Sinica, Taipei 115, Taiwan
Department of Ecology and Evolution, University of Chicago, Chicago, IL 60637, USA
Authors to whom correspondence should be addressed.
Received: 9 April 2012 / Revised: 9 May 2012 / Accepted: 18 May 2012 / Published: 23 May 2012
(This article belongs to the Special Issue Advances in Molecular Oncology (special issue))
View Full-Text   |   Download PDF [785 KB, uploaded 19 June 2014]   |  


microRNAs (miRNAs) cause mRNA degradation or translation suppression of their target genes. Previous studies have found direct involvement of miRNAs in cancer initiation and progression. Artificial miRNAs, designed to target single or multiple genes of interest, provide a new therapeutic strategy for cancer. This study investigates the anti-tumor effect of a novel artificial miRNA, miR P-27-5p, on breast cancer. In this study, we reveal that miR P-27-5p downregulates the differential gene expressions associated with the protein modification process and regulation of cell cycle in T-47D cells. Introduction of this novel artificial miRNA, miR P-27-5p, into breast cell lines inhibits cell proliferation and induces the first “gap” phase (G1) cell cycle arrest in cancer cell lines but does not affect normal breast cells. We further show that miR P-27-5p targets the 3′-untranslated mRNA region (3′-UTR) of cyclin-dependent kinase 4 (CDK4) and reduces both the mRNA and protein level of CDK4, which in turn, interferes with phosphorylation of the retinoblastoma protein (RB1). Overall, our data suggest that the effects of miR p-27-5p on cell proliferation and G1 cell cycle arrest are through the downregulation of CDK4 and the suppression of RB1 phosphorylation. This study opens avenues for future therapies targeting breast cancer. View Full-Text
Keywords: miR P-27-5p; exon array; cyclin-dependent kinase 4; cell cycle; breast cancer; retinoblastoma protein miR P-27-5p; exon array; cyclin-dependent kinase 4; cell cycle; breast cancer; retinoblastoma protein

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Tseng, C.-W.; Huang, H.-C.; Shih, A.-C.; Chang, Y.-Y.; Hsu, C.-C.; Chang, J.-Y.; Li, W.-H.; Juan, H.-F. Revealing the Anti-Tumor Effect of Artificial miRNA p-27-5p on Human Breast Carcinoma Cell Line T-47D. Int. J. Mol. Sci. 2012, 13, 6352-6369.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top