Peter MacCallum Cancer Centre, Melbourne, Australia.
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Australia.
Growth Factors. 2022 Aug;40(3-4):119-152. doi: 10.1080/08977194.2022.2087520. Epub 2022 Jul 21.
Organ-specific metastasis to secondary organs is dependent on the formation of a supportive pre-metastatic niche. This tissue-specific microenvironmental response is thought to be mediated by mutational and epigenetic changes to primary tumour cells resulting in altered cross-talk between cell types. This response is augmented through the release of tumour and stromal signalling mediators including cytokines, chemokines, exosomes and growth factors. Although researchers have elucidated some of the cancer-promoting features that are bespoke to organotropic metastasis to the lungs, it remains unclear if these are organ-specific or generic between organs. Understanding the mechanisms that mediate the metastasis-promoting synergy between the host microenvironment, immunity, and pulmonary structures may elucidate predictive, prognostic and therapeutic markers that could be targeted to reduce the metastatic burden of disease. Herein, we give an updated summary of the known cellular and molecular mechanisms that contribute to the formation of the lung pre-metastatic niche and tissue-specific metastasis.
器官特异性转移到次级器官依赖于支持性的转移前生态位的形成。这种组织特异性的微环境反应被认为是由原发肿瘤细胞的突变和表观遗传改变介导的，导致细胞类型之间的交叉对话发生改变。这种反应通过释放肿瘤和基质信号介质（包括细胞因子、趋化因子、外泌体和生长因子）得到增强。尽管研究人员已经阐明了一些与肺器官特异性转移相关的促进癌症的特征，但尚不清楚这些特征是器官特异性的还是器官间通用的。了解介导宿主微环境、免疫和肺结构之间促进转移协同作用的机制，可以阐明预测、预后和治疗的标志物，这些标志物可以作为靶点，以减少疾病的转移负担。在此，我们对已知的有助于肺转移前生态位形成和组织特异性转移的细胞和分子机制进行了更新总结。
