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Cancer cell plasticity during tumor progression, metastasis and response to therapy

Abstract

Cell plasticity represents the ability of cells to be reprogrammed and to change their fate and identity, enabling homeostasis restoration and tissue regeneration following damage. Cell plasticity also contributes to pathological conditions, such as cancer, enabling cells to acquire new phenotypic and functional features by transiting across distinct cell states that contribute to tumor initiation, progression, metastasis and resistance to therapy. Here, we review the intrinsic and extrinsic mechanisms driving cell plasticity that promote tumor growth and proliferation as well as metastasis and drug tolerance. Finally, we discuss how cell plasticity could be exploited for anti-cancer therapy.

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Fig. 1: Cell plasticity during homeostasis, regeneration and tumorigenesis.
Fig. 2: Defining CSCs and their niche.
Fig. 3: Cell plasticity along the metastatic cascade.
Fig. 4: Molecular mechanisms regulating cancer cell plasticity.
Fig. 5: Genetically induced drug resistance and non-genetic drug tolerance in anti-cancer therapy.

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Acknowledgements

C.B. is supported by WELBIO, the FNRS, TELEVIE, the Fonds Erasme, the Fondation Contre le Cancer, the ULB Foundation, FNRS–FWO EOS and European Research Council advanced grant TTTS. A.P.-G. is supported by the ITN network EVOMET (955951) of the EU Horizon 2020 research and innovation program. K.B. is supported by TELEVIE.

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Pérez-González, A., Bévant, K. & Blanpain, C. Cancer cell plasticity during tumor progression, metastasis and response to therapy. Nat Cancer 4, 1063–1082 (2023). https://doi.org/10.1038/s43018-023-00595-y

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