miRNA-mediated deregulation in leukemia

Dell’Aversana, Carmela; Altucci, Lucia

doi:10.3389/fgene.2012.00252

Cited by 8 publications

(7 citation statements)

References 107 publications

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“…A global imbalance of miRNA expression (and function) was reported in both solid and hematological malignancies 4 including acute myeloid leukemia (AML). 5 AML includes genetically diverse malignancies characterized by frequent chromosome translocations and variable response to treatment. 6 , 7 …”

Section: Introductionmentioning

confidence: 99%

miR-194-5p/BCLAF1 deregulation in AML tumorigenesis

et al. 2017

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Deregulation of epigenetic mechanisms, including microRNA, contributes to leukemogenesis and drug resistance by interfering with cancer-specific molecular pathways. Here, we show that the balance between miR-194-5p and its newly discovered target BCL2-associated transcription factor 1 (BCLAF1) regulates differentiation and survival of normal hematopoietic progenitors. In acute myeloid leukemias this balance is perturbed, locking cells into an immature, potentially ‘immortal’ state. Enhanced expression of miR-194-5p by treatment with the histone deacetylase inhibitor SAHA or by exogenous miR-194-5p expression re-sensitizes cells to differentiation and apoptosis by inducing BCLAF1 to shuttle between nucleus and cytosol. miR-194-5p/BCLAF1 balance was found commonly deregulated in 60 primary acute myeloid leukemia patients and was largely restored by ex vivo SAHA treatment. Our findings link treatment responsiveness to re-instatement of miR-194-5p/BCLAF1 balance.

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Section: Introductionmentioning

confidence: 99%

miR-194-5p/BCLAF1 deregulation in AML tumorigenesis

et al. 2017

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“…miRNA possesses diverse roles that up- or down-regulate target gene expression [ 52 - 57 ]. To identify the miR-130a target genes responsible for its effects on cervical cancer cells, we used bioinformatics and functional knowledge associated with NF-κB and miR-130a and chose TNF-α as a candidate gene for further study.…”

Section: Discussionmentioning

confidence: 99%

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

Zhang

et al. 2014

J Transl Med

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BackgroundNuclear factor-κB (NF-κB) induces a variety of biological processes through transcriptional gene control whose products are components in various signaling pathways. MicroRNAs are a small endogenous non-coding RNAs that regulate gene expression and are involved in tumorigenesis. Using human cervical cancer cell lines, this study aimed to investigate whether NF-κB could regulate miR-130a expression and the functions and targets of miR-130a.MethodsWe used the HeLa and C33A cervical cancer cell lines that were transfected with NF-κB or miR-130a overexpression plasmids to evaluate their effects on cell growth. We utilized bioinformatics, a fluorescent reporter assay, qRT-PCR and Western blotting to identify downstream target genes.ResultsIn HeLa and C33A cells, NF-κB and miR-130a overexpression promoted cell growth, but genetic knockdowns suppressed growth. TNF-α was identified as a target of miR-130a by binding in a 3’-untranslated region (3’UTR) EGFP reporter assay and by Western blot analysis. Furthermore, low TNF-α concentrations stimulated NF-κB activity and then induced miR-130a expression, and TNF-α overexpression rescued the effects of miR-130a on cervical cancer cells.ConclusionsOur findings indicate that TNF-α can activate NF-κB activity, which can reduce miR-130a expression, and that miR-130a targets and downregulates TNF-α expression. Hence, we shed light on the negative feedback regulation of NF-κB/miR-130a/TNF-α/NF-κB in cervical cancer and may provide insight into the carcinogenesis of cervical cancer.

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“…MicroRNAs (miRNAs, miR‐s) are a class of endogenous small, non‐coding RNAs with a length of 22–23 nt RNAs, and could regulate expression of hundreds of target mRNAs simultaneously in a post‐transcriptional manner, thus modulating a variety of cell functions including cell proliferation, differentiation, death, tumor development and also radiosensitivity [Hao et al, ; Liu et al, ; Lin et al, ]. It was also reported that miRNAs might function as tumor suppressor genes and oncogenes [D'Amato et al, ; Dell'aversana and Altucci, ]. For example, dysregulation of the miR‐17‐92 cluster can induce B cell lymphoma while the expressing level of let‐7 is associated with tumor progression and poor prognosis of lung cancer patients [Wang and Lee, ; John‐Aryankalayil et al, ; Shu et al, ; Tian et al, ].…”

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confidence: 99%

Down Regulation of miR200c Promotes Radiation‐Induced Thymic Lymphoma by Targeting BMI1

Cui

Cheng

Zhang

et al. 2014

J of Cellular Biochemistry

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The miR-200c has recently been implicated in the epithelial to mesenchymal transition (EMT) process by directly target the EMT related transcriptional factors ZEB1 and ZEB2. The expression of this miRNA is inversely correlated with tumorgenecity and invasiveness in several human cancers. However, little is known about the expression and targets of the miR-200c in radiation carcinogenesis. Here in this study, using a split radiation induced thymic lymphoma (RITL) model in BALB/c mice, we found that miR-200c is down-regulated in RITL samples. Cell death and apoptosis in lymphoma cells was induced by miR-200c mimic while decreased by miR-200c inhibitor. Computational analysis found a putative target site of miR-200c in the 3'UTR of one of the polycomb group (PcG) protein BMI1 mRNA, which was verified by a luciferase reporter assay. Forced over-expression of miR-200c decreased the level of BMI1 protein and moreover, over-expression of BMI1 rescued the biological effects of miR-200c, indicating BMI1 is a direct mediator of miR-200c functions. Furthermore, the BMI1 expression level was up-regulated and inversely correlated with miR-200c in RITL samples. Finally, our data also indicates that Adenovirus over-expression of pre-miR-200c reduced tumorgenesis in vivo. Taken together, we conclude that down-regulated expression of miR-200c and up-regulation of its direct target BMI1 in radiation-induced thymic lymphoma, which may indicate a novel therapeutic method for RITL through induction of miR-200c or inhibition of BMI1.

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miRNA-mediated deregulation in leukemia

Cited by 8 publications

References 107 publications

miR-194-5p/BCLAF1 deregulation in AML tumorigenesis

miR-194-5p/BCLAF1 deregulation in AML tumorigenesis

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

Down Regulation of miR200c Promotes Radiation‐Induced Thymic Lymphoma by Targeting BMI1

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