Bone metastasis in endocrine-related cancer: unravelling invasion and destruction.

Huong Duong, Georgia Kafer, Michelle Maugham-Macan
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Abstract

Bone is a common and debilitating site for metastatic cancer cell expansion. Skeletal metastasis is a multistage process, with primary stages of circulating tumour cells, progressing to a dormant state in vasculature and bone marrow niches, followed by tumorigenic reactivation, proliferation, and finally bone destruction. The frequency of bone metastasis is reconciled in Paget's "seed and soil" hypothesis, where a conducive microenvironment (bone niche) is essential for cancer cell colonisation. Cancer cells can mimic bone cells (osteomimicry) and interact with the bone marrow's vascular architecture, utilising pathways akin to hematopoietic stem cell expansion. Current research suggests that each phase of bone metastasis is associated with specific gene expression and protein abundance patterns. For example, E-selectin, CXCR-4, and CXCL-12 are crucial for cancer cell homing, dormancy, and colonisation of bone tissue. In contrast, different primary cancers appear to have unique staging profiles. In prostate cancer, dormancy is modulated by the CXCR-4/CXCL-12, ANXA2/CXCL12, and GAS6 pathways, while in breast cancer, dormancy involves ERK1/2, p38, MSK1, LIF, BMP-7, TGF-β1/2, and bone resorption factors. Conversely, osteoblastic metastasis in both breast and prostate cancers is characterised by ET-1, Dkk1 suppression, and the release of IL-6, MCP-1, VEGF, FGF, and IGF, while osteolytic metastasis primarily depends on PTHrP, RANKL, OPG, TGF-β, IGF, TNF-α, IL-1, and IL-7. Understanding the complex molecular mechanisms facilitating cancer cell colonisation and expansion in bone tissues is essential for developing effective treatments to prevent bone metastases . In this review, we discuss current theories linking bone remodelling with bone.

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骨骼是转移性癌细胞扩张的常见和衰弱部位。骨骼转移是一个多阶段的过程,初级阶段是循环肿瘤细胞,然后在血管和骨髓壁龛中进入休眠状态,接着是肿瘤重新激活、增殖,最后是骨质破坏。帕吉特的 "种子与土壤 "假说解释了骨转移的频率,即有利的微环境(骨龛)是癌细胞定植的必要条件。癌细胞可模仿骨细胞(仿骨),并利用类似造血干细胞扩增的途径与骨髓血管结构相互作用。目前的研究表明,骨转移的每个阶段都与特定的基因表达和蛋白质丰度模式有关。例如,E-选择素、CXCR-4 和 CXCL-12 对癌细胞的归巢、休眠和骨组织定植至关重要。相比之下,不同的原发性癌症似乎具有独特的分期特征。在前列腺癌中,休眠受 CXCR-4/CXCL-12、ANXA2/CXCL12 和 GAS6 途径的调节,而在乳腺癌中,休眠涉及 ERK1/2、p38、MSK1、LIF、BMP-7、TGF-β1/2 和骨吸收因子。相反,乳腺癌和前列腺癌的成骨细胞转移则以 ET-1、Dkk1 抑制以及 IL-6、MCP-1、VEGF、FGF 和 IGF 的释放为特征,而溶骨性转移则主要依赖于 PTHrP、RANKL、OPG、TGF-β、IGF、TNF-α、IL-1 和 IL-7。了解促进癌细胞在骨组织中定植和扩展的复杂分子机制对于开发有效的治疗方法以预防骨转移至关重要。在这篇综述中,我们将讨论目前将骨重塑与骨相关联的理论。
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