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Imbalanced expression of polycistronic miRNA in acute myeloid leukemia
Ryutaro Kotaki1, Hiroshi Higuchi1, Daisuke Ogiya2
1Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Abstract:
miR-1 and miR-133 are clustered on the same chromosomal loci and are transcribed together as a single transcript that is positively regulated by ecotropic virus integration site-1 (EVI1). Previously, we described how miR-133 has anti-tumorigenic potential through repression of EVI1 expression. It has also been reported that miR-1 is oncogenic in the case of acute myeloid leukemia (AML). Here, we show that expression of miR-1 and miR-133, which have distinct functions, is differentially regulated between AML cell lines. Interestingly, the expression of miR-1 and EVI1, which binds to the promoter of the miR-1/miR-133 cluster, is correlative. The expression levels of TDP-43, an RNA-binding protein that has been reported to increase the expression, but inhibits the activity, of miR-1, were not correlated with expression levels of miR-1 in AML cells. Taken together, our observations raise the possibility that the balance of polycistronic miRNAs is regulated post-transcriptionally in a hierarchical manner possibly involving EVI1, suggesting that the deregulation of this balance may play some role in AML cells with high EVI1 expression.
Insights
The balance of miR-1 and miR-133 microRNAs is altered in acute myeloid leukemia (AML). Ecotropic virus integration site-1 (EVI1) may regulate this balance, impacting AML development.
Area of Science:
- Molecular Biology
- Cancer Biology
- Genetics
Background:
- MicroRNAs (miRNAs) miR-1 and miR-133 are co-transcribed and play distinct roles in cancer.
- miR-133 exhibits anti-tumorigenic properties by downregulating ecotropic virus integration site-1 (EVI1).
- miR-1 has been implicated as oncogenic in acute myeloid leukemia (AML).
Purpose of the Study:
- To investigate the differential regulation of miR-1 and miR-133 in AML cell lines.
- To explore the relationship between miR-1, miR-133, EVI1, and TDP-43 expression in AML.
- To understand the potential role of miRNA cluster deregulation in AML pathogenesis.
Main Methods:
- Analysis of miR-1 and miR-133 expression levels in AML cell lines.
- Correlation analysis of EVI1 and TDP-43 expression with miR-1 and miR-133 levels.
- Investigation of EVI1 binding to the miR-1/miR-133 promoter.
Main Results:
- Differential expression of miR-1 and miR-133 was observed between AML cell lines.
- A positive correlation was found between miR-1 and EVI1 expression.
- TDP-43 expression levels did not correlate with miR-1 expression in AML cells.
Conclusions:
- The balance of polycistronic miRNAs, like miR-1/miR-133, may be regulated post-transcriptionally, potentially involving EVI1.
- Deregulation of this miRNA balance could contribute to AML, particularly in cases with high EVI1 expression.
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