Abstract
MicroRNAs (miRNAs, or miRs) are single-strand short non-coding RNAs with a pivotal role in the regulation of physiological- or disease-associated cellular processes. They bind to target miRs modulating gene expression at post-transcriptional levels. Here, we present an overview of miRs deregulation in the pathogenesis of multiple myeloma (MM), and discuss the potential use of miRs/nanocarriers association in clinic. Since miRs can act as oncogenes or tumor suppressors, strategies based on their inhibition and/or replacement represent the new opportunities in cancer therapy. The miRs delivery systems include liposomes, polymers, and exosomes that increase their physical stability and prevent nuclease degradation. Phase I/II clinical trials support the importance of miRs as an innovative therapeutic approach in nanomedicine to prevent cancer progression and drug resistance. Results in clinical practice are promising.
Highlights
Multiple myeloma (MM) is an incurable hematologic malignancy characterized by the clonal accumulation of monotypic paraprotein-secreting cells (MM cells) in the bone marrow (BM) [1]
Its pathophysiology depends on different oncogenic events at MM cell level as well as on extracellular factors within the BM microenvironment (BMME) [2]
As a single miR can interact with many mRNAs, miRs simultaneously modulate numerous cellular signaling pathways resulting in cell growth, proliferation, metastasis, and drug resistance [6,7,8]
Summary
Multiple myeloma (MM) is an incurable hematologic malignancy characterized by the clonal accumulation of monotypic paraprotein-secreting cells (MM cells) in the bone marrow (BM) [1]. The miR-29b downregulation is involved in the creation of an immune suppressive BMME that contributes to disease progression This downregulation was found in healthy dendritic cells (DCs) co-cultured with different MM cell lines as well as in CD11c+CD45+ DCs from MM patients versus normal mature DCs. In contrast, increased miR-29b expression counteracts the pro-inflammatory DCs phenotype preventing the intracellular pathways activation, i.e., nuclear factor-κB (NFkB), STAT3, mitogen-activated protein kinase and JUN. We demonstrated that MM cells-derived exosomes contain WWC-2 protein that activates Hippo signaling and induces de novo miRs synthesis in recipient FBs, suggesting the potential role of exosome in reprogramming BMME and miRs expression [51] Overall, these studies support the idea that miRs deregulation is an important step of MM pathogenesis and progression and suggest that they may be envisaged as novel therapeutic management for MM patients
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