Melanoma cell invasiveness is regulated by miR-211 suppression of the BRN2 transcription factor
Boyle, Glen M., Woods, Susan L., Bonazzi, Vanessa F., Stark, Mitchell S., Hacker, Elke, Aoude, Lauren G., Dutton-Regester, Ken, Cook, Anthony L., Sturm, Richard A., & Hayward, Nicholas K. (2011) Melanoma cell invasiveness is regulated by miR-211 suppression of the BRN2 transcription factor. Pigment Cell and Melanoma Research, 24(3), pp. 525-537.
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To identify microRNAs potentially involved in melanomagenesis, we compared microRNA expression profiles between melanoma cell lines and cultured melanocytes. The most differentially expressed microRNA between the normal and tumor cell lines was miR-211. We focused on this pigment-cell-enriched miRNA as it is derived from the microphthalmia-associated transcription factor (MITF)-regulated gene, TRPM1 (melastatin). We find that miR-211 expression is greatly decreased in melanoma cells and melanoblasts compared to melanocytes. Bioinformatic analysis identified a large number of potential targets of miR-211, including POU3F2 (BRN2). Inhibition of miR-211 in normal melanocytes resulted in increased BRN2 protein, indicating that endogenous miR-211 represses BRN2 in differentiated cells. Over-expression of miR-211 in melanoma cell lines changed the invasive potential of the cells in vitro through directly targeting BRN2 translation. We propose a model for the apparent non-overlapping expression levels of BRN2 and MITF in melanoma, mediated by miR-211 expression.
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|Item Type:||Journal Article|
|Keywords:||Invasion, Melanoma, MicroRNA, POU3F2, BRN2|
|Subjects:||Australian and New Zealand Standard Research Classification > BIOLOGICAL SCIENCES (060000) > BIOCHEMISTRY AND CELL BIOLOGY (060100)|
|Divisions:||Current > QUT Faculties and Divisions > Faculty of Health|
Current > Institutes > Institute of Health and Biomedical Innovation
Current > Schools > School of Public Health & Social Work
|Copyright Owner:||Copyright 2011 John Wiley & Sons A/S|
|Deposited On:||07 Dec 2011 09:55|
|Last Modified:||11 Oct 2012 23:21|
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