About this Research Topic
Given the success of Volume I of this Research Topic, and how rapidly the subject area is evolving, we are pleased to announce the launch of Volume II: Characterizing the Multi-faceted Dynamics of Tumor Cell Plasticity.
Cellular plasticity – the ability to dynamically adapt to various changing biochemical and biomechanical intracellular and extracellular conditions – is a hallmark of cancer aggressiveness. Metastasis, tumor relapse, and resistance against various therapies are manifestations of this multi-faceted phenomenon. Modes of cellular plasticity include transitions among phenotypes on the epithelial-mesenchymal spectrum, those with different subsets of cancer stem cells (CSCs) and non-CSCs, those displaying varied metabolic phenotypes and those with various polarizations of macrophages (M1/M2), among others.
Recent in vitro, in vivo, and in silico studies have highlighted that all the above-mentioned processes - Epithelial-to-Mesenchymal Transition (EMT), macrophage polarization, and Warburg effect - are not binary processes as originally hypothesized, instead, cells can acquire one or more hybrid phenotype(s). The hybrid epithelial/mesenchymal (E/M) phenotypes may underpin collective cell migration during metastasis through clusters of circulating tumor cells or emboli and are typically more ‘stem-like’ and aggressive than cells on either end of the spectrum of Epithelial-Mesenchymal Plasticity (EMP). Similarly, hybrid glycolytic/oxidative phosphorylation metabolic phenotypes encompass metabolic plasticity driven aggressiveness. Finally, reversible transitions among non-CSCs and different subsets of CSCs represent a population-level equilibrium maintained among various tumor cell populations. Recent progress in charting the underlying regulatory networks mediating these interconnected manifestations of plasticity have facilitated detailed computational analysis to identify various nodes in these networks that can potentially serve as biomarkers or therapeutic targets. However, a comprehensive characterization of the dynamics of these transitions and other associated traits such as drug resistance, immune evasion, epigenetic modifications, genetic instability, and cell migration and invasion, and identification of the molecular factors that coordinate these associations remains incomplete.
This Research Topic will focus on the molecular and cellular aspects of the multi-dimensional nature of tumor cell plasticity and its implications during various cancer progression, metastasis, and tumor relapse. We welcome investigators to contribute their latest original research articles as well as review articles and perspectives on the characterizing the multifaceted dynamics of cellular plasticity, particularly EMP. Potential topics include but are not limited to:
• Latest technologies to investigate cellular plasticity and heterogeneity in vitro, in vivo, and in silico
• Regulatory networks governing EMP, metabolic reprogramming, stemness, epigenetic, immune evasion, etc.
• Correlation of cell plasticity with various clinical aspects such as disease progression and patient survival
• Molecular mechanisms connecting EMP to metastasis, tumor relapse, and other fibrotic diseases
• Clinical evidence of cellular plasticity and heterogeneity in various pathological conditions
Cellular plasticity – the ability to dynamically adapt to various changing biochemical and biomechanical intracellular and extracellular conditions – is a hallmark of cancer aggressiveness. Metastasis, tumor relapse, and resistance against various therapies are manifestations of this multi-faceted phenomenon. Modes of cellular plasticity include transitions among phenotypes on the epithelial-mesenchymal spectrum, those with different subsets of cancer stem cells (CSCs) and non-CSCs, those displaying varied metabolic phenotypes and those with various polarizations of macrophages (M1/M2), among others.
Recent in vitro, in vivo, and in silico studies have highlighted that all the above-mentioned processes - Epithelial-to-Mesenchymal Transition (EMT), macrophage polarization, and Warburg effect - are not binary processes as originally hypothesized, instead, cells can acquire one or more hybrid phenotype(s). The hybrid epithelial/mesenchymal (E/M) phenotypes may underpin collective cell migration during metastasis through clusters of circulating tumor cells or emboli and are typically more ‘stem-like’ and aggressive than cells on either end of the spectrum of Epithelial-Mesenchymal Plasticity (EMP). Similarly, hybrid glycolytic/oxidative phosphorylation metabolic phenotypes encompass metabolic plasticity driven aggressiveness. Finally, reversible transitions among non-CSCs and different subsets of CSCs represent a population-level equilibrium maintained among various tumor cell populations. Recent progress in charting the underlying regulatory networks mediating these interconnected manifestations of plasticity have facilitated detailed computational analysis to identify various nodes in these networks that can potentially serve as biomarkers or therapeutic targets. However, a comprehensive characterization of the dynamics of these transitions and other associated traits such as drug resistance, immune evasion, epigenetic modifications, genetic instability, and cell migration and invasion, and identification of the molecular factors that coordinate these associations remains incomplete.
This Research Topic will focus on the molecular and cellular aspects of the multi-dimensional nature of tumor cell plasticity and its implications during various cancer progression, metastasis, and tumor relapse. We welcome investigators to contribute their latest original research articles as well as review articles and perspectives on the characterizing the multifaceted dynamics of cellular plasticity, particularly EMP. Potential topics include but are not limited to:
• Latest technologies to investigate cellular plasticity and heterogeneity in vitro, in vivo, and in silico
• Regulatory networks governing EMP, metabolic reprogramming, stemness, epigenetic, immune evasion, etc.
• Correlation of cell plasticity with various clinical aspects such as disease progression and patient survival
• Molecular mechanisms connecting EMP to metastasis, tumor relapse, and other fibrotic diseases
• Clinical evidence of cellular plasticity and heterogeneity in various pathological conditions
Keywords: Cellular plasticity, Tumor cell plasticity, Epithelial/mesenchymal (E/M) phenotypes, Therapeutic targets, Metastasis, Tumor relapse
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
