Journal
SEMINARS IN CANCER BIOLOGY
Volume 53, Issue -, Pages 48-58Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2018.08.009
Keywords
Cancer stem-like cells; EMT; Cancer cell plasticity; Metastasis; Therapy response; Intra-tumor heterogeneity
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Funding
- IDIBELL Fellowship
- Spanish Ministry of Science and Innovation [SAF2014-55944R, SAF2017-84976R]
- Spanish Ministry of Science and Innovation (FEDER funds/European Regional Development Fund (ERDF)-a way to build Europa)
- Catalan Department of Health (Generalitat de Catalunya)
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Most tumors exhibit intra-tumor heterogeneity, which is associated with disease progression and an impaired response to therapy. Cancer cell plasticity has been proposed as being an important mechanism that, along with genetic and epigenetic alterations, promotes cancer cell diversity and contributes to intra-tumor heterogeneity. Plasticity endows cancer cells with the capacity to shift dynamically between a differentiated state, with limited tumorigenic potential, and an undifferentiated or cancer stem-like cell (CSC) state, which is responsible for longterm tumor growth. In addition, it confers the ability to transit into distinct CSC states with different competence to invade, disseminate and seed metastasis. Cancer cell plasticity has been linked to the epithelial-to-mesenchymal transition program and relies not only on cell-autonomous mechanisms, but also on signals provided by the tumor microenvironment and/or induced in response to therapy. We provide an overview of the dynamic transition for cancer cell states, the mechanisms governing cell plasticity and their impact on tumor progression, metastasis and therapy response. Understanding the mechanisms involved in cancer cell plasticity will provide insights for establishing new therapeutic interventions.
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