MicroRNA-206: a Promising Theranostic Marker

Novák, Jan; Kružliak, Peter; Bienertová-Vašků, Julie; Slabý, Ondřej; Novák, Miroslav

doi:10.7150/thno.7552

Cited by 50 publications

(39 citation statements)

References 135 publications

(230 reference statements)

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“…In addition, miR-206 has been shown to have tumor suppression capabilities in other cancer types such as breast cancer, lung cancer, hepatocellular carcinoma, pancreatic adenocarcinoma and others. 26 These studies provide further evidence for the role of miR-206 in decreasing proliferation independent of myogenic differentiation, suggesting miR-206 mimics may be of value as a broad cancer therapy.…”

Section: Discussionmentioning

confidence: 71%

“…21, 22, 23, 24 Furthermore, viral expression of miR-206 in RMS cell line xenografts in mice decreased tumor growth. 22, 25 This recent work has highlighted a few exciting targets of miR-206 in RMS; 26 however, the necessity and/or sufficiency of these putative miR-206 target genes in mediating RMS differentiation remained unexplored. Using a combinatorial approach with microarrays, large-scale proteomics, and prediction algorithms, we identified the crucial miR-206 targets responsible for the developmental arrest in RMS.…”

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confidence: 99%

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PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma

Hanna

Garcia

et al. 2016

Cell Death Dis

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Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood. RMS can be parsed based on clinical outcome into two subtypes, fusion-positive RMS (FP-RMS) or fusion-negative RMS (FN-RMS) based on the presence or absence of either PAX3-FOXO1 or PAX7-FOXO1 gene fusions. In both RMS subtypes, tumor cells show histology and a gene expression pattern resembling that of developmentally arrested skeletal muscle. Differentiation therapy is an attractive approach to embryonal tumors of childhood including RMS; however, agents to drive RMS differentiation have not entered the clinic and their mechanisms remain unclear. MicroRNA-206 (miR-206) expression increases through normal muscle development and has decreased levels in RMS compared with normal skeletal muscle. Increasing miR-206 expression drives differentiation of RMS, but the target genes responsible for the relief of the development arrest are largely unknown. Using a combinatorial approach with gene and proteomic profiling coupled with genetic rescue, we identified key miR-206 targets responsible for the FN-RMS differentiation blockade, PAX7, PAX3, NOTCH3, and CCND2. Specifically, we determined that PAX7 downregulation is necessary for miR-206-induced cell cycle exit and myogenic differentiation in FN-RMS but not in FP-RMS. Gene knockdown of targets necessary for miR-206-induced differentiation alone or in combination was not sufficient to phenocopy the differentiation phenotype from miR-206, thus illustrating that miR-206 replacement offers the ability to modulate a complex network of genes responsible for the developmental arrest in FN-RMS. Genetic deletion of miR-206 in a mouse model of FN-RMS accelerated and exacerbated tumor development, indicating that both in vitro and in vivo miR-206 acts as a tumor suppressor in FN-RMS at least partially through downregulation of PAX7. Collectively, our results illustrate that miR-206 relieves the differentiation arrest in FN-RMS and suggests that miR-206 replacement could be a potential therapeutic differentiation strategy.

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Section: Discussionmentioning

confidence: 71%

mentioning

confidence: 99%

PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma

Hanna

Garcia

et al. 2016

Cell Death Dis

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“…In the last 20 years, since the time of the first discovery and characterization of miRNAs, there has been an explosion of new findings of their contribution to human diseases, and many research efforts have been carried out to find miRNAbased therapeutic and diagnostic approaches [220,221]. In some fields such as oncology, the advance has opened new avenues both for better understanding the pathophysiology of the disease and for implementing potentially innovative treatments [222][223][224].…”

Section: Discussionmentioning

confidence: 98%

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

et al. 2014

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Despite dopamine-glutamate aberrant interaction that has long been considered a relevant landmark of psychosis pathophysiology, several aspects of these two neurotransmitters reciprocal interaction remain to be defined. The emerging role of postsynaptic density (PSD) proteins at glutamate synapse as a molecular "lego" making a functional hub where different signals converge may add a new piece of information to understand how dopamine-glutamate interaction may work with regard to schizophrenia pathophysiology and treatment. More recently, compelling evidence suggests a relevant role for microRNA (miRNA) as a new class of dopamine and glutamate modulators with regulatory functions in the reciprocal interaction of these two neurotransmitters. Here, we aimed at addressing the following issues: (i) Do miRNAs have a role in schizophrenia pathophysiology in the context of dopamine-glutamate aberrant interaction? (ii) If miRNAs are relevant for dopamine-glutamate interaction, at what level this modulation takes place? (iii) Finally, will this knowledge open the door to innovative diagnostic and therapeutic tools? The biogenesis of miRNAs and their role in synaptic plasticity with relevance to schizophrenia will be considered in the context of dopamine-glutamate interaction, with special focus on miRNA interaction with PSD elements. From this framework, implications both for biomarkers identification and potential innovative interventions will be considered.

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“…It has been estimated that they are able to modulate up to 60% of protein-coding genes in the human genome at the translational level [1]. Because of their ubiquitous role in gene regulation, they are involved in many physiological processes, such as differentiation, proliferation, apoptosis and development, and their dysregulation has been related to various pathological disorders, including muscular dystrophy [2], diabetes [3] and several types of cancer [4]. …”

Section: Biogenesis Of Mirnasmentioning

confidence: 99%

MicroRNA in Control of Gene Expression: An Overview of Nuclear Functions

Catalanotto

Cogoni

Zardo

2016

IJMS

1,012

675

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The finding that small non-coding RNAs (ncRNAs) are able to control gene expression in a sequence specific manner has had a massive impact on biology. Recent improvements in high throughput sequencing and computational prediction methods have allowed the discovery and classification of several types of ncRNAs. Based on their precursor structures, biogenesis pathways and modes of action, ncRNAs are classified as small interfering RNAs (siRNAs), microRNAs (miRNAs), PIWI-interacting RNAs (piRNAs), endogenous small interfering RNAs (endo-siRNAs or esiRNAs), promoter associate RNAs (pRNAs), small nucleolar RNAs (snoRNAs) and sno-derived RNAs. Among these, miRNAs appear as important cytoplasmic regulators of gene expression. miRNAs act as post-transcriptional regulators of their messenger RNA (mRNA) targets via mRNA degradation and/or translational repression. However, it is becoming evident that miRNAs also have specific nuclear functions. Among these, the most studied and debated activity is the miRNA-guided transcriptional control of gene expression. Although available data detail quite precisely the effectors of this activity, the mechanisms by which miRNAs identify their gene targets to control transcription are still a matter of debate. Here, we focus on nuclear functions of miRNAs and on alternative mechanisms of target recognition, at the promoter lavel, by miRNAs in carrying out transcriptional gene silencing.

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MicroRNA-206: a Promising Theranostic Marker

Cited by 50 publications

References 135 publications

PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma

PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma

MicroRNAs in Schizophrenia: Implications for Synaptic Plasticity and Dopamine–Glutamate Interaction at the Postsynaptic Density. New Avenues for Antipsychotic Treatment Under a Theranostic Perspective

MicroRNA in Control of Gene Expression: An Overview of Nuclear Functions

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