Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
---|---|---|---|---|---|---|---|---|---|---|---|
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0.070 | Biomarker | disease | BEFREE | MiR-206 is a remarkable miRNA because it functions as a suppressor miRNA in rhabdomyosarcoma while at the same time, as previously showed, it can act as an oncomiRNA in SMARCB1 immunonegative soft tissue sarcomas. | 30111166 | 2018 | ||||
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0.070 | Biomarker | disease | BEFREE | 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. | 27277678 | 2016 | ||||
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0.070 | Biomarker | disease | BEFREE | Thus, HO-1 inhibition activates an miR-206-dependent myogenic program in RMS, offering a novel therapeutic strategy for treatment of this malignancy. | 27488535 | 2016 | ||||
|
0.070 | Biomarker | disease | BEFREE | SMYD1 and G6PD modulation are critical events for miR-206-mediated differentiation of rhabdomyosarcoma. | 25644430 | 2015 | ||||
|
0.070 | Biomarker | disease | BEFREE | Here we show that the BAF53a transcript is significantly higher in primary RMS tumors than in normal muscle, and is a direct target of miR-206. | 23728344 | 2014 | ||||
|
0.070 | Biomarker | disease | BEFREE | In this issue of the JCI, a step toward the realization of this promise is described.Taulli et al. demonstrate that the miRNAs miR-1/miR-206, which are routinely lost in advanced, poorly differentiated rhabdomyosarcoma (RMS) but characteristically expressed in the mature skeletal muscle from which these tumors arise, restore the myogenic differentiation program and block the tumorigenic phenotype (see the related article beginning on page 2366). | 19620782 | 2009 | ||||
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0.070 | AlteredExpression | disease | BEFREE | Finally, we showed that the product of the MET proto-oncogene, the Met tyrosine-kinase receptor, which is overexpressed in RMS and has been implicated in RMS pathogenesis, was downregulated in murine satellite cells by miR-206 at the onset of normal myogenesis. | 19620785 | 2009 |