期刊
CELL STEM CELL
卷 24, 期 1, 页码 65-78出版社
CELL PRESS
DOI: 10.1016/j.stem.2018.11.011
关键词
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资金
- Raymond and Beverly Sackler Convergence Laboratory
- ArtBeCAUSE
- Breast Cancer Research Foundation
- NIH/NICDH [HD073035]
- NIH/NCI [CA170851]
- NIH/GMS [GM124491]
Our traditional understanding of phenotypic plasticity in adult somatic cells comprises dedifferentiation and transdifferentiation in the context of tissue regeneration or wound healing. Although dedifferentiation is central to tissue repair and stemness, this process inherently carries the risk of cancer initiation. Consequently, recent research suggests phenotypic plasticity as a new paradigm for understanding cancer initiation, progression, and resistance to therapy. Here, we discuss how cells acquire plasticity and the role of plasticity in initiating cancer, cancer progression, andmetastasis and in developing therapy resistance. We also highlight the epithelial-to-mesenchymal transition (EMT) and known molecular mechanisms underlying plasticity and we consider potential therapeutic avenues.
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