Expression signatures of intragenic miRNAs and their corresponding host genes in myeloid leukemia cells

Wang, Jing; Xiang, Guangxin; Zhang, Ke; Zhou, Yuxiang

doi:10.1007/s10529-012-1018-0

Cited by 11 publications

(9 citation statements)

References 27 publications

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“…To this end, we inhibited miR-22 in human leukemia cell lines, K562 and U937, both of which express relatively high levels of miR-22 (Figure S5F and Ref. (Wang et al, 2012)), by using a miR-22 retroviral sponge or a custom-made LNA (locked nucleic acid (Petersen and Wengel, 2003)) miR-22 decoy as the miR-22 sponge. Critically, inhibition of miR-22 in human leukemic cells resulted in a significant reduction in cell proliferation as well as an elevation of the expression of TET2 and its targets, AIM2 and SP140 (Figures 6I and 6J and Figures S5G–S5I).…”

Section: Resultsmentioning

confidence: 99%

The Oncogenic MicroRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation

et al. 2013

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SUMMARY MicroRNAs are frequently deregulated in cancer. Here we show that miR-22 is upregulated in myelodysplastic syndrome (MDS) and leukemia, and its aberrant expression correlates with poor survival. To explore its role in hematopoietic stem cell function and malignancy, we generated transgenic mice conditionally expressing miR-22 in the hematopoietic compartment. These mice displayed reduced levels of global 5-hydroxymethylcytosine (5-hmC) and increased hematopoietic stem cell self-renewal, accompanied by defective differentiation. Conversely, miR-22 inhibition blocked proliferation in both mouse and human leukemic cells. Over time, miR-22 transgenic mice developed MDS and hematological malignancies. We also identify TET2 as a key target of miR-22 in this context. Ectopic expression of TET2 suppressed the miR-22-incuced phenotypes. Downregulation of TET2 protein also correlated with poor clinical outcomes and miR-22 overexpression in MDS patients. Our results therefore identify miR-22 as a potent proto-oncogene, and suggest that aberrations in the miR-22-TET2 regulatory network are common in hematopoietic malignancies.

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Section: Resultsmentioning

confidence: 99%

The Oncogenic MicroRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation

et al. 2013

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“…Profilings of miRNAs provide clues to the pathogenesis of MDS The miRNA profiles of various hematological malignancies have been determined, [16][17][18][19] and have been shown to differ. 20 MDS is regarded as a preleukemia disease and a third of MDS patients will develop into AML ultimately 1 .…”

Section: Profilings Of Mirna In Mdsmentioning

confidence: 99%

Deregulated microRNA expression and its pathogenetic implications for myelodysplastic syndromes

2016

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“…The relation of miRNAs with their host genes has been mainly demonstrated for cancer [20][21][22]. Especially those intragenic miRNAs exhibiting a high degree of conservation between species, appear to be coordinately regulated and expressed with their host genes, either with synergistic or antagonistic correlation patterns [23].…”

Section: Introductionmentioning

confidence: 99%

Intragenic MicroRNAs Autoregulate Their Host Genes in Both Direct and Indirect Ways—A Cross-Species Analysis

Zeidler

Hüttenhofer

Kress

et al. 2020

Cells

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MicroRNAs (miRNAs) function as master switches for post-transcriptional gene expression. Their genes are either located in the extragenic space or within host genes, but these intragenic miRNA::host gene interactions are largely enigmatic. The aim of this study was to investigate the location and co-regulation of all to date available miRNA sequences and their host genes in an unbiased computational approach. The majority of miRNAs were located within intronic regions of protein-coding and non-coding genes. These intragenic miRNAs exhibited both increased target probability as well as higher target prediction scores as compared to a model of randomly permutated genes. This was associated with a higher number of miRNA recognition elements for the hosted miRNAs within their host genes. In addition, strong indirect autoregulation of host genes through modulation of functionally connected gene clusters by intragenic miRNAs was demonstrated. In addition to direct miRNA-to-host gene targeting, intragenic miRNAs also appeared to interact with functionally related genes, thus affecting their host gene function through an indirect autoregulatory mechanism. This strongly argues for the biological relevance of autoregulation not only for the host genes themselves but, more importantly, for the entire gene cluster interacting with the host gene.

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Expression signatures of intragenic miRNAs and their corresponding host genes in myeloid leukemia cells

Cited by 11 publications

References 27 publications

The Oncogenic MicroRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation

The Oncogenic MicroRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation

Deregulated microRNA expression and its pathogenetic implications for myelodysplastic syndromes

Intragenic MicroRNAs Autoregulate Their Host Genes in Both Direct and Indirect Ways—A Cross-Species Analysis

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