2023
DOI: 10.3389/fnetp.2023.1225736
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Quantifying cancer cell plasticity with gene regulatory networks and single-cell dynamics

Sarah M. Groves,
Vito Quaranta

Abstract: Phenotypic plasticity of cancer cells can lead to complex cell state dynamics during tumor progression and acquired resistance. Highly plastic stem-like states may be inherently drug-resistant. Moreover, cell state dynamics in response to therapy allow a tumor to evade treatment. In both scenarios, quantifying plasticity is essential for identifying high-plasticity states or elucidating transition paths between states. Currently, methods to quantify plasticity tend to focus on 1) quantification of quasi-potent… Show more

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Cited by 2 publications
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“…This happens due to a ’one-to-many’ gene interaction rather than a ’one-to-one’ interaction, facilitated by cell-state transitions and network switching. Similar to cancer cell metastasis 53, 54 , the dynamic network switching of genes may allow reversible phenotypic plasticity (cell-state transition), causing resistance to drug and survival benefits to the cells. Next, we focused on identifying the subset of genes with the strongest control in the entire network and the potential roles of the key genes (Table S1) in the network at different time points.…”
Section: Resultsmentioning
confidence: 99%
“…This happens due to a ’one-to-many’ gene interaction rather than a ’one-to-one’ interaction, facilitated by cell-state transitions and network switching. Similar to cancer cell metastasis 53, 54 , the dynamic network switching of genes may allow reversible phenotypic plasticity (cell-state transition), causing resistance to drug and survival benefits to the cells. Next, we focused on identifying the subset of genes with the strongest control in the entire network and the potential roles of the key genes (Table S1) in the network at different time points.…”
Section: Resultsmentioning
confidence: 99%