Phenotypic plasticity - Implications for tumours in bone

被引:4
|
作者
Han, Yujiao [1 ]
Kang, Yibin [1 ,2 ,3 ]
机构
[1] Princeton Univ, Dept Mol Biol, Lewis Thomas Lab 255,Washington Rd, Princeton, NJ 08544 USA
[2] Ludwig Inst Canc Res, Princeton Branch, Princeton, NJ USA
[3] Canc Inst New Jersey, Canc Metab & Growth Program, New Brunswick, NJ USA
关键词
PROSTATE-CANCER CELLS; BREAST-CANCER;
D O I
10.1016/j.jbo.2024.100592
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Metastasis is a major contributor to cancer patient mortality. Tumour cells often develop phenotypic plasticity to successfully metastasize to different target organs. Recent progress in the study of bone metastasis has provided novel insight into the biological processes that drive the spread and growth of cancer cells in the bone. In this review, we provide a summary of how the bone marrow microenvironment promotes phenotypic plasticity of metastatic tumour cells and alters therapeutic responses. We highlight pivotal transformations in cellular status driven by plasticity, including mesenchymal-epithelial transition, acquisition of stem -like traits, and awakening from dormancy. Additionally, we describe the phenomenon of host -organ mimicry and metabolic rewiring that collectively serve as key attributes of disseminated tumour cells, enabling their successful colonization and growth within the bone marrow microenvironment.
引用
收藏
页数:4
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