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首页> 外文期刊>Cell cycle >Metalloproteinases and osteoblast EGFR signaling in osteolytic bone metastasis of breast cancer.
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Metalloproteinases and osteoblast EGFR signaling in osteolytic bone metastasis of breast cancer.

机译：金属蛋白酶和成骨细胞EGFR信号转导在乳腺癌的溶骨性转移中。

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Bone is among the most frequent targets of distant metastasis for breast cancer. Most bone lesions in breast cancer patients are of osteolytic nature, i.e., destruction of bone accompanies the growth of tumors. Bone metastasis severely reduces the quality of life for cancer patients with debilitating and life-threatening complications such as bone fracture, bone pain, nerve compression and hypercalcemia. Recent studies have revealed that bone metastasis is controlled by the complex interactions between tumor cells and several resident cell types in the bone microen-vironment, in particular, the bone-building osteoblasts and the bone-degrading osteoclasts. A fine balance of osteoblast and osteoclast activities is essential for bone homeostasis and is carefully maintained in part through paracrine signaling between these two cell types. Osteoblasts produce receptor activator of nuclear factor KB ligand (RANKL) that stimulates the differentiation of osteoclasts from their precursors. Meanwhile, osteoblasts also express osteoprotegerin (OPG), a decoy receptor and antagonist of RANKL. Appropriate RANKL/OPG ratio is crucial for maintaining a healthy level of bone remodeling and for avoiding pathological conditions such as osteoporosis or osteopetrosis. Tumor cells disrupt the molecular program of bone homeostasis by producing signaling proteins, such as parathyroid hormone-related pep-tide (PTHrP), that stimulate osteoblasts to upregulate RANKL or downregulate OPG, ultimately promoting osteoclast differentiation and activity. Identifying additional tumor-derived molecules that engage bone stromal cells in the pathological process of osteolytic bone metastasis holds promise for controlling the disease.
机译：骨是乳腺癌远距离转移的最常见靶标之一。乳腺癌患者中的大多数骨病变具有溶骨性质，即，骨破坏伴随肿瘤的生长。骨转移严重降低患有衰弱和危及生命的并发症（例如骨折，骨痛，神经压迫和高钙血症）的癌症患者的生活质量。最近的研究表明，骨转移受肿瘤细胞与骨骼微环境中几种驻留细胞类型（特别是造骨成骨细胞和降解骨的破骨细胞）之间复杂的相互作用控制。成骨细胞和破骨细胞活性的良好平衡对于骨骼的体内平衡至关重要，并且通过这两种细胞类型之间的旁分泌信号传导得以仔细维护。成骨细胞产生核因子KB配体（RANKL）的受体激活剂，刺激破骨细胞与其前体的分化。同时，成骨细胞还表达了RANKL的诱饵受体和拮抗剂osteoprotegerin（OPG）。适当的RANKL / OPG比对于维持健康的骨骼重塑水平和避免诸如骨质疏松症或骨质疏松症等病理状况至关重要。肿瘤细胞通过产生信号蛋白（如甲状旁腺激素相关肽（PTHrP））来破坏骨稳态的分子程序，该蛋白刺激成骨细胞上调RANKL或下调OPG，最终促进破骨细胞的分化和活性。在溶骨性骨转移的病理过程中鉴定参与骨基质细胞的其他肿瘤衍生分子有望控制该疾病。

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