Abstract
Bone remodeling is uncoupled in the multiple myeloma (MM) bone marrow niche, resulting in enhanced osteoclastogenesis responsible of MM-related bone disease (MMBD). Several studies have disclosed the mechanisms underlying increased osteoclast formation and activity triggered by the various cellular components of the MM bone marrow microenvironment, leading to the identification of novel targets for therapeutic intervention. In this regard, recent attention has been given to non-coding RNA (ncRNA) molecules, that finely tune gene expression programs involved in bone homeostasis both in physiological and pathological settings. In this review, we will analyze major signaling pathways involved in MMBD pathophysiology, and report emerging evidence of their regulation by different classes of ncRNAs.
Highlights
Multiple myeloma bone disease (MMBD) is a hallmark feature of multiple myeloma (MM), the second most common hematological malignancy characterized by abnormal proliferation of monoclonal plasma cells (PCs) in the bone marrow (BM)
Bone remodeling under pathological conditions is characterized by a strong inhibition of OBs activity, which leads to bone loss as OBs are unable to repair the lesions caused by the excessive osteoclastic resorption; the latter process is strongly supported by MM cells, which can exacerbate OCs activity promoting their maturation directly or by physically interacting with other cellular components, such as the BM stromal cells (BMSCs)
We will briefly discuss the signaling pathways implicated in the development of MM-related bone disease (MMBD), and, will analyze how they are modulated by manipulation or release of non-coding RNA (ncRNA) from different bone marrow microenvironment (BMM) cells
Summary
Multiple myeloma bone disease (MMBD) is a hallmark feature of multiple myeloma (MM), the second most common hematological malignancy characterized by abnormal proliferation of monoclonal plasma cells (PCs) in the bone marrow (BM). Bone remodeling under pathological conditions is characterized by a strong inhibition of OBs activity, which leads to bone loss as OBs are unable to repair the lesions caused by the excessive osteoclastic resorption; the latter process is strongly supported by MM cells, which can exacerbate OCs activity promoting their maturation directly or by physically interacting with other cellular components, such as the BM stromal cells (BMSCs). To effectively trigger BD, cellular components of the BMM produce and/or secrete a number of functional molecules, which collectively contribute to the osteoclastogenic events. In this regard, non-coding RNAs (ncRNAs) have recently emerged as fine regulators of gene expression programs underlying key molecular events featuring bone remodeling in MM. We will briefly discuss the signaling pathways implicated in the development of MMBD, and, will analyze how they are modulated by manipulation or release of ncRNAs from different BMM cells
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