Vermont Cancer Center and Department of Biochemistry, University of Vermont College of Medicine, Burlington, Vermont.
J Cell Physiol. 2014 Dec;229(12):1884-6. doi: 10.1002/jcp.24692.
Skeletal metastasis is a serious complication of many primary cancers. A common feature of tumor cells that metastasize to the bone marrow microenvironment is that they initiate a cascade of events, recruiting and presumably/potentially altering the phenotype of bone marrow mesenchymal stromal cells (MSC) to produce an environment that allows for tumor growth and in some cases, drug-resistant dormancy of latent cancer cells. Consequently the MSC population can contribute to metastatic disease through several distinct mechanisms by differentiating into cancer-associated fibroblasts (CAFs). Understanding the expression and epigenetic changes that occur as normal MSCs become associated with metastatic tumors would reveal possible therapeutic targets for treating skeletal metastasis.
骨骼转移是许多原发性癌症的严重并发症。转移到骨髓微环境的肿瘤细胞的一个共同特征是，它们引发级联事件，招募并可能改变骨髓间充质基质细胞（MSC）的表型，产生允许肿瘤生长的环境，在某些情况下，还会使潜伏癌细胞产生耐药性休眠。因此，MSC 群体可以通过几种不同的机制分化为癌相关成纤维细胞（CAFs），从而促进转移性疾病的发展。了解正常 MSC 与转移性肿瘤相关时发生的表达和表观遗传变化，将揭示治疗骨骼转移的可能治疗靶点。
