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Characterization of global microRNA expression reveals oncogenic potential of miR-145 in metastatic colorectal cancer
Authors
A Jemal
A Paredes-Zaglul
+51 more
A Provenzani
AJ Schetter
Angela Lai
Anton Bittner
BP Lewis
C Chen
Chunyan Zhang
D Tsafrir
E Bandres
E Berezikov
E Bernstein
E Lund
E Staub
EA Wiemer
ER Fearon
G Lanza
GA Calin
GJ Liefers
Greg M Arndt
Hongtao Fan
J Lu
J Shingara
J Weitz
JM Cummins
JT Mendell
Kathy Retzlaff
Lara M Cullen
LD Wood
Lesley Dossey
Michael Eisbacher
Mitch Raponi
MZ Michael
Nham Tran
NS Williams
PH Rooney
R Yi
RC Bates
Riki Druker
S Volinia
SM Hammond
T Schepeler
T Sjoblom
TW Nilsen
U Alon
Y Akao
Y Akao
Y Gusev
Y Lee
Y Lee
Y Wang
Y Xi
Publication date
1 January 2009
Publisher
BioMed Central
Doi
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on
PubMed
Abstract
Background: MicroRNAs (MiRNAs) are short non-coding RNAs that control protein expression through various mechanisms. Their altered expression has been shown to be associated with various cancers. The aim of this study was to profile miRNA expression in colorectal cancer (CRC) and to analyze the function of specific miRNAs in CRC cells. MirVana miRNA Bioarrays were used to determine the miRNA expression profile in eight CRC cell line models, 45 human CRC samples of different stages, and four matched normal colon tissue samples. SW620 CRC cells were stably transduced with miR-143 or miR-145 expression vectors and analyzed in vitro for cell proliferation, cell differentiation and anchorage-independent growth. Signalling pathways associated with differentially expressed miRNAs were identified using a gene set enrichment analysis. Results: The expression analysis of clinical CRC samples identified 37 miRNAs that were differentially expressed between CRC and normal tissue. Furthermore, several of these miRNAs were associated with CRC tumor progression including loss of miR-133a and gain of miR-224. We identified 11 common miRNAs that were differentially expressed between normal colon and CRC in both the cell line models and clinical samples. In vitro functional studies indicated that miR-143 and miR-145 appear to function in opposing manners to either inhibit or augment cell proliferation in a metastatic CRC model. The pathways targeted by miR-143 and miR-145 showed no significant overlap. Furthermore, gene expression analysis of metastatic versus non-metastatic isogenic cell lines indicated that miR-145 targets involved in cell cycle and neuregulin pathways were significantly down-regulated in the metastatic context. Conclusion: MiRNAs showing altered expression at different stages of CRC could be targets for CRC therapies and be further developed as potential diagnostic and prognostic analytes. The identified biological processes and signalling pathways collectively targeted by co-expressed miRNAs in CRC provide a basis for understanding the functional role of miRNAs in cancer. © 2009 Arndt et al; licensee BioMed Central Ltd
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