Figure 2. Diagram summarizing the mechanism by which miR-3140-3p overcomes the acquired resistance to BETi in NB cells (IMAGE)
Caption
Activated ERK1/2 stabilizes MYCN protein by preventing ubiquitin-mediated proteolysis via phosphorylation of MYCN at Ser62 in BETi-acquired resistant NB cells, thereby attenuating the effects of BETi in these cells. miR-3140-3p efficiently downregulated MYCN expression by directly targeting the MAP3K3-ERK1/2 pathway in addition to BRD4 suppression, inhibiting tumor cell growth in BETi-acquired resistant NB cells.
Credit
Department of Molecular Cytogenetics, TMDU
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