Abstract
Osteolytic bone metastasis frequently occurs in the later stages of breast, lung, and several other cancers. Osteoclasts, the only cells that resorb bone, are hijacked by tumor cells, which break down bone remodeling systems. As a result, osteolysis occurs and may cause patients to suffer bone fractures, pain, and hypercalcemia. It is important to understand the mechanism of bone metastasis to establish new cancer therapies. MicroRNAs are small, noncoding RNAs that are involved in various biological processes, including cellular differentiation, proliferation, apoptosis, and tumorigenesis. MicroRNAs have significant clinical potential, including their use as new therapeutic targets and disease-specific biomarkers. Recent studies have revealed that microRNAs are involved in osteoclast differentiation and osteolytic bone metastasis. In this review focusing on microRNAs, the author discusses the roles of microRNAs in osteoclastogenesis and osteolytic bone metastasis.
Highlights
Cancer is one of the most common causes of death, and bone is the third most common cancer metastatic site following the lung and liver [1]
Osteoclastogenesis is regulated by a variety of hormones, growth factors, and cytokines, macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κB ligand (RANKL), which are expressed in stromal cells and osteoblasts, are essential for osteoclast differentiation [5,6]
transforming growth factor β (TGF-β) released from the matrix as a result of increased bone resorption can cause tumor cells to produce growth factors such as parathyroid hormone-related protein (PTHrP) and interleukin 11 (IL-11) that can perturb the RANKL/OPG balance, resulting in further osteoclastogenesis and perpetuation of osteolytic disease [2] (Figure 2)
Summary
Cancer is one of the most common causes of death, and bone is the third most common cancer metastatic site following the lung and liver [1]. Patients with metastasis to bone often present with lesions that can be osteoblastic, osteolytic, or a mixture of the two [2]. Osteolytic bone metastasis is caused by excessive osteoclast activity relative to osteoblast activity [2]. Osteoclastogenesis is regulated by a variety of hormones, growth factors, and cytokines, macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κB ligand (RANKL), which are expressed in stromal cells and osteoblasts, are essential for osteoclast differentiation [5,6]. RANKL/RANK induces c-Fos to form activator protein-1 (AP-1), a heterodimeric transcription factor, with c-Jun. AP-1 and NF-κB induce nuclear factor of activated T cell cytoplasmic 1 (NFATc1), a master transcription factor that regulates osteoclast differentiation.
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